Aliment Pharmacol Ther 2005; 22: 685–700.
Systematic review: tuberculous peritonitis – presenting features,
diagnostic strategies and treatment
F. M. SANAI & K. I. BZEIZI
Division of Hepatology, Department of Internal Medicine, Riyadh, Saudi Arabia
Accepted for publication 27 July 2005
SUMMARY
The peritoneum is one of the most common extrapulmo-
nary sites of tuberculous infection. Peritoneal tuberculo-
sis remains a significant problem in parts of the world
where tuberculosis is prevalent. Increasing population
migration, usage of more potent immunosuppressant
therapy and the acquired immunodeficiency syndrome
epidemic has contributed to a resurgence of this disease in
regions where it had previously been largely controlled.
Tuberculous peritonitis frequently complicates patients
with underlying end-stage renal or liver disease that
further adds to the diagnostic difficulty.
The diagnosis of this disease, however, remains a
challenge because of its insidious nature, the variability
of its presentation and the limitations of available
diagnostic tests. A high index of suspicion is needed
whenever confronted with unexplained ascites,
particularly in high-risk patients.
INTRODUCTION
The first documented case of ancient ‘tuberculosis (TB)
peritonitis’ was described in humans in 1843.1 Intro-
duction of antituberculous chemotherapy and more
importantly, the improvement in the socioeconomic
status, led to a decline in all forms of TB, including
tuberculous peritonitis (TBP). Although abdominal TB
continues to be a significant health problem in the
Correspondence to: Dr F. M. Sanai, Division of Hepatology (A41),
Department of Internal Medicine, Armed Forces Hospital, PO Box 7897,
Riyadh 11159, Saudi Arabia.
E-mail: faisalsanai@hotmail.com

2005 Blackwell Publishing Ltd
doi: 10.1111/j.1365-2036.2005.02645.
Based on a systematic review of the literature, we
recommend: tuberculous peritonitis should be consid-
ered in the differential diagnosis of all patients present-
ing with unexplained lymphocytic ascites and those
with a serum-ascites albumin gradient (SAAG) of
<11 g/L; culture growth of Mycobacterium of the ascitic
fluid or peritoneal biopsy as the gold standard test;
further studies to determine the role of polymerase
chain reaction, ascitic adenosine deaminase and the
BACTEC radiometric system for acceleration of myco-
bacterial identification as means of improving the
diagnostic yield; increasing utilization of ultrasound
and computerized tomographic scan for the diagnosis
and as a guidance to obtain peritoneal biopsies; low
threshold for diagnostic laparoscopy; treatment for
6 months with the first-line antituberculous drugs
(isoniazid, rifampicin, ethambutol and pyrazinamide)
in uncomplicated cases.
developing world, recently there has been an increase in
the number of patients diagnosed with abdominal TB in
parts of the world where TB generally was rare. This is
partly a result of increasing travel and migration and
also to the rising number of HIV patients who are
susceptible to opportunistic infections.2 There has been
a cumulative evidence of relative increase in the
incidence of the extrapulmonary TB.3–5
Abdominal TB may involve the gastrointestinal tract,
peritoneum or the mesenteric lymph nodes. Occasional
overlaps between these forms have also been described.
Peritoneum and its reflections are common sites of
tuberculous involvement of the abdomen and it is the
685
686 F. M. SANAI AND K. I. BZEIZI
sixth most common extrapulmonary site in the United
States.5 It occurs in up to 3.5% of cases of pulmonary
TB and comprises 31–58% of cases of abdominal TB.6–9
In western Europe and North America, a frequent
association between TBP and cirrhosis has been des-
cribed.10–12 Other groups of patients at increased risk of
developing TBP include chronic renal failure patients on
continuous ambulatory peritoneal dialysis (CAPD) and
HIV patients.13, 14 Several reports have also highlighted
the remarkable similarity between this illness and
ovarian carcinoma,15 carcinomatosis peritonii16 and
complicated portal hypertensive ascites.
The diagnosis of this disease continues to pose
significant challenges. This is partly due to the lack of
specific clinical features that would otherwise help in
pursuing the diagnosis when suspected and also to the
limited yield of the commonly used diagnostic tests.
Isolation of mycobacteria from the ascitic fluid is difficult
and frequently laparoscopy is needed for the diagnosis.
In this review we aim to address the variability of
disease presentation, the associated risk factors of the
disease and will review the current knowledge of the
diagnostic measures available and treatment options.
Search strategy for identification of studies
We reviewed the literature available on this subject by
performing a Medline search limited to the English
language (January 1966–October 2004). The search
terms used were: ‘tuberculous peritonitis’, ‘peritoneal
tuberculosis’, ‘tuberculosis and ascites’, ‘abdominal
tuberculosis’ and ‘tuberculosis and laparoscopy’.
Abstracts of the articles selected in each of these multiple
searches were identified and those dealing particularly
with the subject were recorded and reviewed in full form.
Reference lists from trials previously selected by elec-
tronic searching were manually searched to identify
further relevant trials. Other publications known to the
authors were also reviewed. In addition, we electronic-
ally scanned major gastroenterology journals for the
most recent studies dealing with the subject. Studies
including paediatric subjects were not excluded.
EPIDEMIOLOGY
The reported incidence of TBP among all forms of TB
varies from 0.1% to 0.7% worldwide.17 Both sexes are
equally affected and the disease is seen most commonly
in patients between 35 and 45 years of age.

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
Variable methods have been used to study TB world-
wide and this might explain the discrepancies of data
available. Increasing migration and also the constant
changes of disease pattern are other factors that made
accurate assessments of the extent of this disease even
more complex. Examples of the methods used to study
TB prevalence include, mortality data, tuberculin skin
test and field surveillance by chest X-ray and sputum
cultures. BCG vaccination has limited the usefulness of
tuberculin skin testing in the diagnosis of TB because a
significant proportion of vaccinated but uninfected
patients will return a positive skin reaction.18 Similarly,
deriving meaningful epidemiological data on this dis-
ease by Mantoux skin testing has also become difficult
because of the vaccination programmes undertaken in
the third world. This trend is observed across all age
groups where non-vaccinated subjects had lower rates
of positive Mantoux test in uninfected patients than
those who had received BCG vaccination.18 The peak
prevalence of a positive skin reaction in those who had
previously been vaccinated occurs in 70% for the age
groups between 45 and 64 years. It is expected that the
rate of positive skin test for future generations will be
significantly higher as current immunization pro-
grammes in most of the third world countries include
BCG vaccination at child-birth. The newly developed
interferon (IFN)-c-based test would help overcome this
problem of detecting latent infection since previous BCG
vaccination does not affect its results.19 However, at
present there is no large-scale epidemiological data
available utilizing this test.
A significant correlation exists between the socioeco-
nomic status and disease prevalence. Poor hygiene and
overcrowding have consistently been shown to have a
causative relationship with TB. Ingestion of unpas-
teurized milk might also be another reason for the
increased prevalence of this disease in the rural
populations. On the contrary, the effective tuberculin
testing of dairy herds and a shift from the norm of
drinking unpasteurized milk in cities, has most likely
contributed to the overall reduction in cases of primary
abdominal TB.
Alcoholic liver disease (ALD) is frequently linked to
increased incidence of TBP particularly in the western
countries. In one study, 62% of patients with TBP had
an underlying ALD,10 a contrast to the findings of
studies from developing countries where the reported
underlying liver diseases was found in <13% of patients
with TBP.20–23
 SYSTEMATIC REVIEW: TUBERCULOUS PERITONITIS
The recent dramatic increase in the number of TB
cases globally is linked to the HIV/AIDS pandemic.24
About 9% of all new TB cases (31% in Africa) in adults
were attributable to HIV/AIDS.24 TB accounts for about
13% of all HIV-related deaths worldwide.24, 25
The incidence of extrapulmonary TB in Unites States
over a 5-year period has risen to 20% compared with
the incidence of 3% for pulmonary TB.26 Of the
5.1 million HIV patients in India, about half of them
are co-infected with TB.27 In India, it is estimated that
15–20% of all TB cases are extrapulmonary in site
amongst the HIV-negative adult population.28 Simi-
larly, Saudi Arabia reported increasing rates of extra-
pulmonary TB (abdominal TB 16%) from 1993 at
which point the incidence was 1.7 cases per 100 000
population, to 4.7 cases in 1997. During the same time
frame, reported pulmonary TB was decreasing.29
PATHOGENESIS
Infection of the peritoneum is usually secondary to
haematogenous spread of tubercles from a pulmonary
focus. Although an abnormal chest X-ray (CXR) is
frequently seen, however coexistent active pulmonary
disease is rare30 (Table 2). Spread of the mycobacteria
may rarely occur from lesions in the adjacent organs
such as the intestine or the fallopian tubes. Intestinal TB
occurs as a result of ingesting contaminated milk or
from swallowing the sputum of active lung disease.31
Alcoholic liver disease is a significant risk factor of
developing TBP.10–12 Shakil et al. found that alcohol
was the underlying cause in 90% of patients with
cirrhosis who developed TBP.10 The mechanism behind
the increased susceptibility of ALD patients to this
disease remains unknown. Unlike spontaneous bacterial
peritonitis, factors such as impaired opsonization,
complement deficiency, low immunoglobulin levels in
the ascitic and low serum albumin level do not appear
to explain the onset of TBP, which is related to impaired
cell-mediated immunity. Also, there is no evidence to
suggests that the impaired humoral immunity of
cirrhosis would play any role in the evolution of this
opportunistic infection. Theoretically, the presence of
stagnant ascitic fluid could potentially predispose to the
onset of opportunistic infections, as might be the case
with patients on CAPD. Against that is the fact that
cellular immunity is impaired in patients with uraemia
and this would be a likely explanation for the increased
susceptibility to TB. Tuberculosis is more common in

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
687
haemodialysis patients than in patients undergoing
CAPD (28% vs. 4.8%),13, 32, 33 which further negates
the hypothesis that the stagnant ascitic fluid is a
significant risk factor of TBP.
Malnutrition frequently develops in cirrhotic patients
and is more prominent in patients ALD due to a number
of reasons. Previous studies have documented the
poorer nutritional health of patients with ALD in
comparison with non-alcoholics.34 Additionally, these
patients demonstrate cutaneous anergy to a variety of
antigens, suggesting impaired T cell-dependent func-
tions, and this immune defect is again more commonly
seen in ALD compared with cirrhosis from other
causes.35 Therefore, it is likely that an interaction
between immunological dysfunction and malnutrition
produces the higher prevalence of TBP in patients with
cirrhosis.
The HIV infection is the strongest of all known risk
factors for the development of TB. HIV patients have
impaired Th1 type immune response, a crucial defence
against Mycobacterium tuberculosis.36, 37 The interaction
between TB and HIV is synergistic. The relative risk of
death and development of other opportunistic infections
is higher in the HIV–TB co-infected patients when
compared with CD4+ count-matched HIV-infected
controls without TB.38
CLINICAL MANIFESTATIONS
TBP is a subacute disease and its symptoms evolve over
a period of several weeks to months. Presence of
comorbid conditions such as cirrhosis result in atypical
presentations that may lead to delayed diagnosis.
Elderly patients with TBP may manifest minimal
constitutional symptoms, which again might cause a
delay in the diagnosis. The disease can present in three
different forms which are: the wet-ascitic, fibrotic-fixed
and the dry-plastic form.39 They have similar clinical
manifestations except for abdominal distension which
does not occur in the dry-plastic form. A considerable
degree of overlap does occur, whereby more than one
form may coexist. The clinical features of this illness
from 35 different studies of TBP have been tabulated
and presented in Table 1. Systemic and constitutional
symptoms are common. Low-grade fever occurs in
about 59% of the cases and it is usually accompanied by
night sweats. Patients may not report fever and in 49%
of the cases it is only documented during hospitaliza-
tion.7, 11, 40 Other systemic features of the disease
688 F. M. SANAI AND K. I. BZEIZI

Table 1. Cumulative data of clinical features compiled from 35 studies of tuberculous peritonitis (TBP)

Clinical feature Number of cases Average (%)

Abdominal pain 12841, 7, 11–13, 15, 20–23, 39–41, 44, 45, 47, 51, 52, 60, 94–104 64.5
Fever 13931, 7, 10–13, 20–23, 40, 41, 44, 45, 47, 51, 52, 60, 94–105 59
Weight loss 7741, 7, 10–13, 20–23, 39–41, 51, 52, 95–99, 106 61
Diarrhoea 6301, 7, 11, 12, 21, 23, 40, 94, 96, 98, 104 21.4
Constipation 31911, 12, 21, 40, 47 11
Ascites 14051, 7, 10–12, 15, 20–23, 39, 40, 41, 44, 45, 47, 51, 52, 94–105, 107
73
Abdominaltenderness 3297, 11, 12, 20, 22, 40, 94–96 47.7
Hepatomegaly 3197, 10–12, 20, 39, 40, 95, 103 28.2
Splenomegaly 18910, 11, 39, 40, 52, 103 14.3

include weight loss, anorexia and malaise. The super-
imposition of this illness on other chronic conditions-
like uraemia, cirrhosis and AIDS make these symptoms
more difficult to quantify. Weight loss is seen in about
61% of cases and investigators have reported reversi-
bility of this manifestation as one of the markers of
disease resolution.7
Abdominal pain is a common presenting symptom and
frequently accompanied by abdominal distension. It is
usually non-localized and vague in nature. The pain is
largely due to the tuberculous inflammation of the
peritoneum and mesentery. Less often, it could be a
manifestation of intermittent subacute intestinal
obstruction, a result of matted bowel loops caused by
adhesions of the mesentery and omentum. The matted
bowel loops could be felt as palpable masses on
abdominal examination. Abdominal symptoms such as
vomiting, diarrhoea and constipation are uncommon.
The pathophysiology of diarrhoea is unknown and it is
very unlikely to be due to direct intestinal involvement
as TBP rarely occurs simultaneously with tuberculous
enteritis.1, 11, 41 Khuroo and Khuroo42 suggested that
the stagnation in dilated segments of intestinal loops
caused by adhesions between mesentery and small
bowel may result in small bowel bacterial overgrowth.
The evidence for this plausible mechanism is however,
not yet available.
Tenderness on palpation is common in TBP and occurs
in almost 48% of the cases and this might help in
differentiating it from spontaneous bacterial perito-
nitis, which complicates portal hypertensive ascites.43
Rebound tenderness is rare as the presence of ascitic
fluid prevents approximation of the parietal with the
visceral peritoneum.
Ascites is the predominant finding and it is present in
about 73% of the patients. A smaller percentage of
patients (5–13%) present with the classical ‘doughy’
abdomen. This is described as the dry or plastic type of
TBP and the patients have very little ascites, which can
only be detected by ultrasonography or during laparos-
copy.39, 44 The ascitic fluid is usually straw coloured, and
although red blood cells are frequently seen on micro-
scopic examination, however, frank haemorrhagic fluid
is seen only in 9% of the cases.21 The dialysate fluid of
patients on CAPD becomes cloudy upon infection with
TBP and this could be the earliest sign of the infection.
Interestingly, from the cumulative data of six large series
compiled by Marshall, it evolved that in 18% of patients,
ascites was detected primarily by radiological means or at
the time of surgery.30 The inaccuracy of detecting ascites
combined with the vague nature of the abdominal pain
and the paucity of other abdominal signs may errone-
ously cause the condition to be mislabelled as a mental
illness. Therefore, a high index of suspicion is required in
diagnosing these patients and a liberal utilization of
imaging studies may be warranted.
An enlarged liver or splenomegaly is uncommon
(Table 1), and presence of hepatomegaly suggests a
direct involvement of the liver.7 Splenomegaly is likely
to reflect presence of portal hypertension. Hepato-
splenomegaly is common in patients with an underlying
ALD except in advanced cirrhosis which results in a
shrunken liver.10, 11, 40
DIAGNOSIS
The insidious nature of this disease makes the diagnosis
a clinical challenge. With the ever-increasing demogra-
phic shift, more cases are now seen in areas of the world
where TB was a rarity. Unless a high degree of suspicion
is maintained, the diagnosis can easily be missed or
inappropriately delayed. The indolent nature of this

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700

 SYSTEMATIC REVIEW: TUBERCULOUS PERITONITIS 689

disease was illustrated by the recent case series, which
consistently reported a prolonged period of symptoms
before the diagnosis was established.13, 45–47 In areas of
high prevalence, it is a routine practice to screen for
Mycobacterium by the special staining and culture of
the ascitic fluid. It would be impractical to perform
this test routinely in areas of the world where TBP is
rare except of course in cases where TB is considered
in the differential diagnosis. The reported incidence
of TBP as a cause for ascites is only 2%.48 However,
the index of suspicion should be high if the patient
has lived or traveled from an endemic area. The same
applies for patients with ALD and those who are
immunosuppressed or undergoing CAPD. Patients with
ascites who have an abnormal CXR or had prior
exposure to open TB should also be screened for
TB.17, 40 The sensitivity patterns of various tests used
to diagnose TBP have been compiled in a tabulated form
based on the cumulative data of 39 series.
Laboratory investigations
Haematological indices. Changes of haematological indi-
ces are non-specific and therefore of little diagnostic
yield. Mild to moderate normochromic, normocytic
anaemia and thrombocytosis are frequent find-
ings.10, 21, 30 The white cell count (WBC) is usually
normal but, lymphomonocytosis is not uncommon.11, 21
The erythrocyte sedimentation rate is almost always
raised but in at least 50% of the cases, the values do not
exceed 60 mm/h.21 Raising the cut-off value does not
alter the specificity of this test as patients with ascites in
general may have similarly raised values.
Ascitic fluid analysis. Ascitic fluid analysis is routinely
performed in evaluating all patients presenting with
ascites. The WBC in TBP varies widely ranging from
counts of <100 cells/mm3 to as high as 5000 cells/
mm3.10, 13 Most patients however, have cell counts
between 500 and 1500 cells/mm3. The cells are
predominantly lymphocytes with the possible exception
of patients with underlying renal failure where, for
unknown reasons, the cells are mostly neutrophils.13, 49
As such, the possibility of TBP cannot be negated in the
presence of a neutrophil-predominant ascitic fluid. The
cumulative data from 13 series of TBP reviewed by us
(Table 2) showed lymphocytic predominance in 68% of
patients. A lymphocytic predominance may also be seen
in portal hypertensive ascites at the end of diuresis or
immediately after antibiotic therapy in previously
unrecognized spontaneous bacterial peritonitis. The
presence of lymphomonocytic ascites therefore is not a
reliable marker for TB and should be considered merely
as an indication for further investigations.
Ascitic fluid biochemistry. Ascitic glucose values is repor-
ted to be slightly low in some studies10, 11 however, there
is no sufficient evidence to support routine ascitic fluid
glucose measurement in patients with suspected TBP.
Ascitic lactate dehydrogenase (LDH) has been reported to
be high in some studies. The ascitic fluid concentration of
LDH is usually less than half of the serum level in

Table 2. Sensitivity patterns of various diagnostic tests from the cumulative data of 39 studies of TBP

Diagnostic Sensitivity
test (%) Remarks

Abnormal CXR 38 1002 patients with TBP1, 10–13, 20–22, 39–41, 44, 45, 47, 51, 52, 60, 94–96, 98–101
Positive PPD 53.16 380 patients studied;10, 11, 20–22, 39, 40, 51, 52, 96 authors used various induration sizes for positivity
Ascitic fluid tests
Predominant lymph 68.34 477 patients;10, 11, 13, 20, 23, 40, 41, 44, 45, 47, 51, 61, 96 investigators had differing definitions
for predominance
LDH 77 87 patients;10, 11, 51, 52 investigators used varying LDH range
ADA (>30 U/L) 94 1305 patients studied; 205 with TBP11, 39, 61, 62, 108–114 Hillebrand et al.61 used >7 U/L as cut-off
Smear 2.93 615 patients1, 10–13, 20–23, 41, 47, 51, 52, 95, 100, 101, 103, 104, 114–118
Culture 34.75 446 patients;1, 10–13, 20, 22, 23, 51, 52, 85, 95, 96, 99–101, 103, 104, 114–116, 118 studies using
BACTEC radiometric system not included
Laparoscopy
Visual diagnosis 92.7 397 patients;10, 20, 21, 23, 39, 51, 119–122
most series did not report specificity
Histology 93 402 patients;10, 20–23, 39, 51, 96, 119–121
patients with intent-to-biopsy included

TBP, tuberculous peritonitis; CXR, chest X-ray; LDH, lactate dehydrogenase; ADA, adenosine deaminase.

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700

690 F. M. SANAI AND K. I. BZEIZI
uncomplicated cirrhotic ascites. In infection, including
TBP, the ascitic fluid LDH level rises because of the release
of LDH from neutrophils. Shakil et al.10 showed that
raised LDH above 90 U/L carries a sensitivity of 90% and
a specificity of 14% for TBP. Such high degree of
sensitivity was not reproduced by another similar
study.11 Data tabulated by us from four different studies
(Table 2) suggest a sensitivity of 77% for LDH. Raised
ascitic LDH with similar degrees of sensitivity also occur
in patients with peritoneal carcinomatosis, pancreatic
ascites and about 20% of those with cirrhosis or
congestive cardiac failure.50 It does appear therefore that
ascitic LDH measurement is not of discriminatory value
and should not necessary be used routinely.
Ascitic fluid proteins. Ascitic fluid total protein levels
>25 g/L is seen in almost 100% of patients with iso-
lated TBP. However, the sensitivity of this test is
significantly reduced (42–70%) when TBP complicates
cirrhosis.10, 11, 51, 52 Ascitic fluid total protein >25 g/L is
found in 100% of nephrogenous ascites,53 22% of
cirrhotics, almost 100% of cardiac ascites50, 54 and 95%
of peritoneal carcinomatosis.54 The serum-ascites albu-
min gradient (SAAG) has more diagnostic yield than
ascitic fluid total protein measurement.50 It is calculated
by measuring both serum and ascitic fluid albumin on
the same day and subtracting the ascitic albumin from
the serum one. A low SAAG (<11 g/L) is seen in 100%
of patients with TBP, although the specificity remains
low.10, 51, 52, 54 Moreover, the sensitivity is greatly
reduced (29–88%) when TBP complicates chronic liver
disease leading to further diagnostic confusion.10, 51
The main advantage of calculating the SAAG is in its
specificity for portal hypertension induced ascites. SAAG
of 11 g/L or greater indicates portal hypertension with
97% of accuracy.54 This is of great significance as
majority of ascites is due to portal hypertension and
therefore specific investigation for other aetiologies such
as TB could be applied to a small group of patients with
unexplained ascites.
Elevation of CA-125 has been documented in the
majority of patients with TBP and created consider-
able confusion by mimicking advanced ovarian carci-
noma.15, 52 Subsequently, this test was recommended
as an indirect marker for TBP. Recent reports have
shown that serum and ascitic CA-125 levels are
elevated in almost all patients with ascites regardless
of the underlying cause.55–57 Patients commenced on
antituberculous treatment have shown rapid falls in

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
CA-125 levels paralleling clinical response and reso-
lution of ascites. Based on the available evidence, this
test does not seem to offer any particular advantage
in the diagnosis of TBP.
Microbiological diagnosis
Ziehl–Neelsen (ZN) staining of the ascitic fluid for
mycobacterial detection is positive in only about 3% of
cases with proven TBP (Table 2). To allow for the
detection of mycobacteria in stained smears, presence of
at least 5000 bacilli/mL of specimen is required,
whereas for positive culture as few as 10 organisms
might be sufficient for the diagnosis.58, 59 The current
‘gold standard’ for the diagnosis of TB entails culturing
the mycobacteria from clinical specimens. Culture
methods based on a combination of liquid or biphasic
media, together with solid media, are used to ensure
maximum sensitivity of detection. Studies reporting on
the microbiological diagnosis have used varied report-
ing methodology. While most have reported on the
regular method of culturing 10–50 mL of ascitic fluid,
others have recommended culturing 1 L of centrifuged
fluid. This is based on the above principle of increasing
yield by increasing the concentration of the bacilli.
Culture of the fluid by the regular method is positive in
35% based on our cumulative data comprising of 446
patients from 22 case series (Table 2), although the
yield has been shown to significantly improve (66–83%)
when 1 L of fluid is centrifuged and then cultured,
either by traditional culture media or the BACTEC
system.41, 47, 60 In clinical practice this is not practical
as the biggest available aliquots for centrifugation have
a capacity of 50 mL. This problem is further compoun-
ded by the 4–8 weeks requirement by the conventional
culture media. The recently introduced BACTEC radio-
metric system is a rapid method for detecting mycobac-
teria in clinical specimens, with a mean time to
detection of 14 days, and can be used to complement
conventional methods.47 A further 7 days are required
for drug susceptibility testing. Other newer methods of
identifying mycobacteria isolates include liquid chro-
matography and DNA probes for which the typical
turnaround time for confirmation is 21 days. Although,
the concept of culturing a litre of centrifuged ascitic fluid
is attractive, it may not be feasible in the regular clinical
setting. Hence, at least in resource-rich settings, the
BACTEC radiometric system should be made available
in routine clinical practice.
 SYSTEMATIC REVIEW: TUBERCULOUS PERITONITIS
New diagnostic tools
Adenosine deaminase. With the persisting diagnostic
difficulties surrounding TBP, there has been an ongoing
search for alternative rapid and non-invasive tests.
Amongst these, adenosine deaminase (ADA) activity in
the ascitic fluid has been studied the most. ADA is an
aminohydrolase that converts adenosine to inosine and
its activity is more in T than in B lymphocytes, this
being proportional to the degree of T-cell differentiation.
ADA is increased in tuberculous ascitic fluid because of
the stimulation of T cells by the mycobacterial antigens.
Sensitivity and specificity levels over 90% have been
reported (Table 2) with the exception of a study by
Hillebrand et al.61 who reported a sensitivity of 59%.
They postulated that their lower sensitivity may have
been related to the higher incidence of cirrhosis in their
group of patients. These observations were countered by
Burgess et al.62 when they evaluated cirrhotic patients
with TBP in their study and reported a sensitivity of
94%, comparable with the findings of previous studies.
This study also demonstrated that raising the ADA level
above 30 U/L did not affect either the sensitivity or the
diagnostic efficiency of this test. At present, an ascitic
ADA activity of ‡30 U/L is generally accepted as the
cut-off level expected to yield the best results. Given its
high rate of diagnostic accuracy and easy availability,
we do recommend increasing the utilization of this test
in the diagnostic work-up of patients with suspected
TBP.
Gene amplification. Another technological advancement
has been the introduction of rapid amplification-based
tests for detecting specific regions of bacterial DNA or
RNA. The polymerase chain reaction (PCR) is a
technique that uses nucleic acid amplification to detect
M. tuberculosis in body tissues. Reports suggest that the
performance of the various PCR tests is reasonably
good with sensitivity reaching up to 95% in smear-
positive patients. The same success has not been
duplicated in smear-negative patients and the sensitiv-
ity attained has been disappointingly low (48%).63 As
the ZN stain in patients with TBP is positive in only
3%, these figures suggest that PCR sensitivity would be
similarly very low. To date, excluding a few case
reports there are no controlled studies of PCR in
patients with TBP.64–66 The issue of false-positives as a
result of cross-contamination of samples has raised
concerns of over-diagnosing TB in areas of endemicity.

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
691
Samples from sites with a possible latent infection
focus or DNA from dead bacilli may also give a positive
reaction.
The ligase chain reaction (LCR) DNA amplification
method has recently been introduced into practice. This
assay has been shown to provide valuable and rapid
information for the diagnosis of extrapulmonary TB and
with a higher diagnostic accuracy than PCR.67 Further
studies are needed to determine the clinical use of PCR
and/or LCR in the diagnosis of TBP. The cost of utilizing
these techniques will be another major issue to consider
particularly in poor countries where TB is endemic.
Immunodiagnostic tests. The search for reliable, repro-
ducible and specific serological tests for the diagnosis of
TBP has been an area of active research for many years.
Various antigens have been targeted in numerous
studies, however few have dealt with the issue of TBP.
In a South African study dealing with active disease, an
enzyme-linked immunosorbent assay to detect IgG to a
43 kDa antigen of M. tuberculosis found it to be highly
sensitive (approaching 100%) and 97% specific for
pleural and ascitic fluids.68 In another report from
India, the seropositivity of the IgA and IgG antibody
directed against A60 antigen was 88.4% in active
gastrointestinal TB.69 However, it is unclear from the
methodology if any of these 26 patients had TBP. High
IFN-c levels in tuberculous ascites have been reported to
be useful diagnostically.70 Although such assays hold
great potential, concerns remain regarding costs, low
positive predictive value and the ability to distinguish
from atypical mycobacterial infection.
Tuberculin skin test
The utilization of tuberculin skin testing has become
controversial and perhaps redundant. Various studies
from different parts of the world have reported positivity
rates ranging between 24 and 100%, and averaging at
53% based on the reported figures of 10 studies (Table 2).
A breakdown along demographic lines of high and low
endemicity areas did not reveal any differences in these
rates. Surprisingly, studies arising from the same regions
have revealed vast differences in their rates of positivi-
ty.20, 51, 52 Possible explanations for this may be linked to
the method of testing, strength of the reagent utilized and
the methodology of interpretation by the investigators in
different studies. Unfortunately, none of these study offer
any of these details. Generally, about 47% of patients with
692 F. M. SANAI AND K. I. BZEIZI
TBP would have false-negative reactions to tuberculin
skin testing.
As the tuberculin skin test has many potential sources
of error and variability, it has become imperative to
standardize the reagent, reading of the test itself, and
the interpretations derived. Recent recommendations by
the American Thoracic Society and the US Centers for
Disease Control and Prevention have placed the cut
point for the induration for those at low risk at 15 mm;
in people at moderate risk the cut point is 10 mm and
those at high risk the cut point is 5 mm.71 Additionally,
the issue of tuberculin testing has shifted away from
detecting active TB to one of screening for latent
infection. Some studies dealing with TBP have
addressed the issue of anergy testing reported to be
positive in about 9% of the cases.10 Anergy testing was
proposed initially to measure the overall ability to
mount a delayed-type hypersensitivity response. How-
ever, anergy testing as a routine adjunct to tuberculin
testing is no longer recommended as it may yield
misleading information.
Despite the high specificity of this test (between 95 and
99%), the low sensitivity, and the low positive predictive
value of 50–67% should obviate the clinician from
placing undue importance to this test.72 Skin testing is
now consigned to detecting latent infection and there
are no recommendations for using this test to diagnose
active disease like TBP. Diagnosis of TB is a clinical
responsibility and tuberculin skin testing, at best, offers
only auxiliary support.
A major scientific advance in detecting latent infection
has been the development of an IFN-c-based test which
yielded a sensitivity of 89%.19 Interferon-c test is a
quantitative in vitro assay that evaluates the cell-
mediated immune response to M. tuberculosis. The test
is based upon the principle that previously sensitized T
lymphocytes release IFN-c in response to stimulation by
purified protein derivative (PPD). This assay has been
shown to have excellent agreement with tuberculin skin
testing. A novel assay that is not widely available, it
measures the amount of IFN-c released by T lympho-
cytes following exposure to the antigen ESAT-6 (nor-
mally absent in BCG) and may be useful for diagnosing
latent TB in patients previously vaccinated with BCG.
Imaging studies
Various studies have reported an abnormal CXR in
19–83% of cases averaging to about 38% based on our

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
cumulative data of over 1000 patients (Table 2). Active
concomitant pulmonary disease however, occurs in
only 14% of patients.30 Although TBP represents one of
the disseminated forms of TB, miliary shadowing is
rarely seen or even reported in the literature. Aguado
et al.,11 found miliary mottling in only one patient out of
20 who had an abnormal CXR.
Ultrasound (US) changes include echogenic debris seen
as fine mobile strands or particulate matter within the
ascitic fluid. Calcifications in the walls of encysted
ascitic fluid are rare and when present, could be
detected by US imaging.73–76
The ascitic fluid has high attenuation values on
computerized tomographic (CT) imaging (20–45 HU).
The peritoneum is commonly thickened and nodular
(Figure 1).73, 75, 77 The fibrotic-fixed type of TBP is
characterized by a hypervascular peritoneum, matting
of the loops, and omental masses. CT seems more
capable of delineating omental changes which occur
in 36–82% of cases.74, 75, 77–80 Thickened mesentery
(>15 mm) with mesenteric lymph nodes is seen in
most cases and this combination may be an early sign
of abdominal TB.81 Loss of normal mesenteric confi-
guration is better demonstrated by CT scan.74, 75, 77, 80
Several studies have compared US and CT findings
in TBP and found them to be complementary to each
other as they provide different information. US is
superior to CT in revealing the multiple, fine, mobile
septations characteristically found in TBP, while CT
can highlight the peritoneal, mesenteric or omental
involvement.75, 82 Ha et al.80 reported 69% sensitivity
in the diagnosis of TBP by CT scan. On the contrary,
another group analysed retrospectively the CT images
of their TBP patients over a 3-year period and found
that the disease had been missed in all cases.83 The
CT abnormalities described above might be seen in
other diseases with peritoneal infiltration notably
peritoneal carcinomatosis. The presence of a smooth
peritoneum with minimal thickening and pronounced
enhancement on CT suggests TBP, whereas nodular
implants and irregular peritoneal thickening suggests
carcinomatosis.
Imagining modalities are increasingly used to help in
obtaining peritoneal biopsies. They provide a safer and
inexpensive alternative to diagnostic laparoscopy. Ear-
lier reports had suggested limited diagnostic sensitiv-
ity59, 83 but a recent report by Vardareli et al.
demonstrated a high diagnostic yield approaching
95% and without any complications.52 This is of vital
 SYSTEMATIC REVIEW: TUBERCULOUS PERITONITIS
Figure 1. A computerized tomographic
(CT) image of a 34-year-old male with fever
and abdominal pain showing a thickened
peritoneum (arrow) with mild ascites. His-
tology was consistent with tuberculous
peritonitis (TBP).
importance for centres with limited laparoscopic avail-
ability or expertise.84
Laparoscopy
Laparoscopy is the diagnostic tool of choice in patients
with suspected TBP. Not only does it allows inspection
of the peritoneum but also offers the option of obtaining
specimens for histology. The well-described laparoscopic
appearance by Bhargava et al.39 classifies it into three
types: thickened, hyperaemic peritoneum with ascites
and whitish miliary nodules (<5 mm) scattered over the
parietal peritoneum (Figure 2), omentum and bowel
loops (66%); thickened and hyperaemic peritoneum
with ascites and adhesions (21%); markedly thickened
parietal peritoneum with possibly yellowish nodules and
cheesy material along with multiple thickened adhe-
sions (fibro-adhesive type – 13%). The diagnostic yield
of laparoscopic examination is very high with a
sensitivity of the macroscopic appearances approaching
93%. The cumulative data of 402 patients from 11
studies (Table 2) showed impressive sensitivity and
specificity rates of 93% and 98% respectively when
the macroscopic appearances are combined with the
histological findings (epitheliod granulomata with case-
ation or mycobacterial identification).
Peritoneal biopsies should always be examined when-
ever possible for culture and sensitivity. It is the gold
standard test that provides diagnostic accuracy and

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
693
helps in optimizing the selection of the anti-TB
therapy. Surprisingly, few studies from the ones that
we reviewed did report results of mycobacterial culture
on specimens obtained at laparoscopy. ZN stain was
positive 3–25%10, 11, 39 while the yield of culture
sensitivity was between 38 and 92%.10, 39, 85
Peritoneal carcinomatosis, sarcoidosis, starch perito-
nitis and Crohn’s disease may occasionally mimic the
laparoscopic features of TBP, hence the importance of
taking biopsies. Granulomatous changes might be seen
in sarcoidosis or Crohn’s disease, however presence of
caseating changes would support the diagnosis of TB.
Complications of laparoscopy are rare, seen in <3% of
cases including bleeding, infection and bowel perfora-
tion. The reported mortality is up to 0.04%.86–88 The
procedure requires expertise and should only be per-
formed by competent surgeons. Moreover, this proce-
dure requires hospitalization and is more expensive
than image-guided peritoneal biopsy.
Failure to obtain tissue for microbiological or histolog-
ical assessment should not deter us from initiating
treatment as studies have consistently reported a
specificity in excess of 96% on the laparoscopic
appearance alone.17 At present there are no random-
ized-controlled trials comparing image guided biopsy,
laparoscopy and laparotomy; and the high number of
patients required would make such a trial unlikely
in the near future. We believe that laparotomy is
unnecessary and is only considered for patients with the
694 F. M. SANAI AND K. I. BZEIZI
fibro-adhesive type of TBP when there is an indication
for a peritoneal biopsy. Although the ideal diagnostic
test requires the demonstration of mycobacteria, how-
ever, the characteristic laparoscopic appearance itself,
even in the absence of bacteriological confirmation,
would be sufficient grounds for the diagnosis of TBP.
TREATMENT
The treatment of TBP is solely pharmacological. The
available data strongly suggest that regimens, which
are curative for pulmonary TB, are also sufficient for
TBP. There are currently five drugs that are considered
first-line medications: isoniazid (INH), rifampicin (RIF),
pyrazinamide (PZA), ethambutol (EMB) and streptomy-
cin (SM). Thiacetazone is widely used in the developing
world because of its low cost, but has substantial
toxicity and limited efficacy. In most circumstances, the
treatment regimen for adult patients with previously
untreated TB should consist of a 2-month initial phase
of INH, RIF, PZA and EMB given on a daily basis. This is
followed by a continuation phase where INH and RIF
are again given on a daily basis for another 4 months.89
There are various second-line drugs-like rifabutin,
fluoroquinolones, ethionamide, aminosalicylic acid and
cycloserine. The treatment of TBP in HIV-infected adults
is the same as that of HIV-uninfected patients, except for
the INH-rifapentine once weekly, continuation phase
which is contraindicated because of high relapse

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
Figure 2. Laparoscopic image of an 18-
year-old girl with fever and ascites showing
multiple whitish nodules (<5 mm) covering
the peritoneum. The biopsy was consistent
with caseating granuloma and acid-fast
bacilli (courtesy: N. Azzam and
A. K. Al-Aska).
rates.89 However, because HIV-infected patients are
often taking multiple medications, some of which may
interact with antituberculous ones, it is strongly
encouraged that experts in the treatment of HIV-related
TB be consulted.
Response to therapy is manifested by resolution of
symptoms and disappearance of ascites. All laboratory-
based tests of disease activity return to normal values,
usually within 3 months of treatment initiation. The
rate of drug resistance varies in different countries and
within different ethnic or regional denominations.
Overall primary resistance rates to standard first-line
medications in low prevalence areas tends to be below
5%, whereas multidrug resistance rates as high as 48%
have been described in high prevalence areas such as
Nepal.90 Drug resistance occurs usually when there is a
large bacillary population, or when an inadequate drug
regimen is prescribed. It also occurs as a result of
malabsorption of the antituberculous drug(s). As the
type of drugs used in resistant forms need to be modified
(along with an extension of the duration of treatment),
conducting drug sensitivities to the organism is essen-
tial. This should not forestall initiation of treatment
because the drugs can be modified as the sensitivity
patterns become available. In the presence of resistance
to first-line therapy, a single drug should not be added to
the failing regimen. Revising therapy in such instances
should be attempted with at least three unused drugs
(one of whom is injectable) to which there is in vitro
 SYSTEMATIC REVIEW: TUBERCULOUS PERITONITIS 695

Clinical features suggestive

Ascites present Ascites absent

Neutrophil
SAAG ≥11 g/L dominant
Imaging Studies
Spontaneous bacterial
Ascitic fluid Lymphocyte peritonitis Rx
analysis dominant
Peritoneal Peritoneal
disease (+) disease (-)
SAAG <11 g/L

IGPB
ADA < 30 ADA > 30 IU/L
IU/L Histology Histology
conclusive inconclusive

TB culture TB culture
negative positive Laparotomy

Anti-TB
Malignant treatment
cells positive

Appearance Appearance
suggestive; suggestive;
histology histology
inconclusive conclusive

Figure 3. Algorithm for evaluation of

patients with suspected tuberculous
Laparoscopy
peritonitis (TBP).

susceptibility. Usage of drugs with demonstrated in vitro
resistance is not encouraged. It is also preferable to use
hospital-based or directly observed therapy.89
Delay in treatment initiation can lead to significant
mortality. Chow et al.47 reported a considerable deteri-
oration in clinical condition of more than 80% of
patients during the diagnostic work-up. The overall
mortality in this study was 35%, while in the subset of
patients with underlying cirrhosis was 73%. Average
mortality from the cumulative data of 18 series
comprising of more than 800 patients was 19%.17
Although, current recommendation for treatment dur-
ation in TBP is only for 6 months, most reported studies
have given treatment for 12 months. There is however,
no evidence to support a recommendation of treatment
beyond 6 months. Some studies that used the 6- or
9-month regimen found almost all of their patients
responded equally to the treatment.51, 52 One study
compared different durations of treatment (9 months to
beyond 12 months) and found no difference in outcome
in either group.11 As such, 6 months of phased therapy
with the standard first line of antituberculous medica-
tions would be adequate for the treatment of TBP.
Role of corticosteroids
Corticosteroids reduce the polymorphonuclear inflam-
matory response, and decrease the peripheral blood
lymphocytes, monocytes, eosinophils and basophils. The
inflammatory fibrotic process of the disease results in
adhesions and subsequent intestinal obstruction.
Adjunctive steroids may offer benefit by minimizing
the inflammation and preventing the postinflammatory
fibrosis. Early trials showed that when corticosteroids
were given in combination with antituberculous med-
ications there was no progression of the TB.91 Over the
decades, this has prompted four trials of adjuvant
corticosteroids use in TBP and all of them cited modest
benefit.40, 51, 60, 85 Alrajhi et al.85 reported considerably
low morbidity and complications in those treated with
corticosteroids. There is a pending need for prospective,
well-controlled clinical trials with long-term follow-ups
to identify the category of patients most likely to benefit
from such therapy. Based on the limited data available,
it is presently difficult to make any firm recommenda-
tions regarding steroid use in TBP patients.
Drug-induced hepatotoxicity
One of the main concerns of clinicians in treating TB is
the hepatotoxic effect of the antituberculous drugs. The
risk is higher in patients with cirrhosis that is commonly
associated with TBP. Asymptomatic elevation of aspar-
tate transaminase (AST) occurs in 20% of patients with
the standard 4-drug regimen for pulmonary TB.92
According to recent recommendations by the American

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700

696 F. M. SANAI AND K. I. BZEIZI
Thoracic Society, Centers for Disease Control and
Infectious Disease Society of America, in such situations
drug therapy need not be altered but the frequency
of clinical and laboratory monitoring should be
increased.89 Stoppage of treatment is recommended if
AST is elevated fivefolds; or threefolds in the presence of
symptoms.89 An increase in bilirubin or alkaline
phosphatase is also a serious adverse event. Restarting
treatment should be attempted when AST values are
less than twofolds and the drug to be introduced first is
RIF, followed by introductions of INH and PZA a week
apart. Asides from this, it is important to consider other
causes of impaired liver functions such as the pre-
existing liver disease or less commonly, direct dissem-
ination of TB to the liver.
Pre-existing liver disease
The treatment of TBP in patients with background liver
disease is problematic. The incidence of drug-induced
hepatitis may be greater and the implications of
hepatotoxicity for patients with cirrhosis are potentially
serious. One study of patients with TB and underlying
liver disease used INH, RIF, EMB and ofloxacin for
2 months followed by INH and RIF for 10 months and
found 0% hepatotoxicity in this group, while another
cohort utilizing a standard regimen developed hepato-
toxicity in 26%.93 The aforementioned recent recom-
mendations89 suggested using any of the following four
regimens in such a scenario.
1 RIF, PZA and EMB for 6 months.
2 INH, RIF, EMB for 2 months followed by INH and
RIF for another 7 months.
3 RIF, EMB, a fluoroquinolone, cycloserine/injectible
agents for 12–18 months.
4 EMB, SM, a fluoroquinolone and another second-line
oral drug.
CONCLUSION
Peritoneal TB remains a common problem in parts of
the world where TB is prevalent. The incidence
worldwide is likely to increase, largely as a consequence
of population migrations, increased immunosuppres-
sant therapy and the AIDS epidemic. Patients with
underlying cirrhosis particularly of alcoholic aetiology
are at higher risk of developing this infection. The risk is
also relatively higher in chronic renal failure patients on

2005 Blackwell Publishing Ltd, Aliment Pharmacol Ther 22, 685–700
CAPD. The diagnosis of this disease requires a high
index of suspicion because of the subtle nature of the
symptoms and signs. TBP should be considered in the
differential diagnosis of all patients presenting with a
lymphocytic ascites and those with a SAAG of <11 g/L.
Ascitic fluid analysis is non-specific and culture growth
of the Mycobacterium remains the ‘gold standard’ for
diagnosis. Ascitic ADA is a relatively new test with
excellent sensitivity and specificity patterns. Further
studies are needed to determine its role as a diagnostic
tool for TBP. Lately, the advent of molecular biology
techniques has led to the introduction of rapid amplifica-
tion-based tests like PCR and LCR. These are yet to be
tested in patients with TBP. The BACTEC radiometric
system for acceleration of mycobacterial identification
does increase the diagnostic yield and we recommend its
wider introduction in clinical practice. Ultrasound and CT
scan are increasingly used for the diagnosis of TBP and
could help in providing guided peritoneal biopsies. Lapar-
oscopy, however, remains the best means of diagnosing
the disease, either by visualization alone or in combination
with biopsy and histological examination. It should be
considered at an early stage whenever TBP is suspected.
It is essential to recognize that a combination of
different diagnostic tests is used in order to arrive at the
diagnosis of TBP. There is no single test that can
consistently yield a diagnosis by itself. Selective screen-
ing of ascitic fluid samples by more defining tests along
with laparoscopic visualization; or histological and
microbiological analysis of tissue obtained would be
required for definitive disease diagnosis in most cases.
The algorithm (Figure 3) outlines the suggested
investigational plan of patients with TBP.
Six months of treatment with the usual first-line
antituberculous drugs is considered sufficient in uncom-
plicated cases.
ACKNOWLEDGEMENT
The authors thank Drs MA Al-Karawi and Al-Barrak
for critically reviewing the manuscript.
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