Clinics and Research in Hepathology and Gastroenterology (2011) 35, 60—69

SEMINAR

Peritoneal tuberculosis
La tuberculose péritonéale

A. Guirat a,∗, M. Koubaa b, R. Mzali a, B. Abid a, S. Ellouz c, N. Affes a,

M. Ben Jemaa b, F. Frikha a, M. Ben Amar a, M.I. Beyrouti a

a
Service de chirurgie générale, CHU Habib Bourguiba, 3029 Sfax, Tunisia
b
Service des maladies infectieuses, CHU Hédi Chaker, 3029 Sfax, Tunisia
c
Service d’anatomie pathologique, CHU Habib Bourguiba, 3029 Sfax, Tunisia

Available online 6 January 2011

Summary The peritoneum is one of the locations outside the most common pulmonary tuber-
culosis. Peritoneal tuberculosis poses a public health problem in endemic regions of the world.
The phenomenon of migration, the increased use of immunosuppressive therapy and the epi-
demic of AIDS have contributed to a resurgence of this disease in regions where it was previously
controlled. The aim of this review is to expose the clinical, biologic end radiologic futures of
the peritoneal tuberculosis and to present the methods of diagnosis and treatment. The diag-
nosis of this disease is difficult and still remains a challenge because of its insidious nature,
the variability of presentation and limitations of available diagnostic tests. The disease usually
presents a picture of lymphocytic exudative ascites. There are many complementary tests with
variable sensitivities and specificities to confirm the diagnosis of peritoneal tuberculosis. Isola-
tion of mycobacteria by culture of ascitic fluid or histological examination of peritoneal biopsy
ideally performed by laparoscopy remains the investigation of choice. The role of PCR, ascitic
adenosine deaminase, interferon gamma and the radiometric BACTEC system can improve the
diagnostic yield. An antituberculous treatment with group 1 of the WHO for 6 months is sufficient
in most cases.
© 2010 Elsevier Masson SAS. All rights reserved.

Résumé Le péritoine est l’une des localisations extrapulmonaire les plus fréquentes de
la tuberculose. La tuberculose péritonéale pose un problème de santé publique dans cer-
taines régions endémiques du monde. Le phénomène de migration, l’utilisation plus fréquente
d’immunosuppresseurs et l’épidémie du sida ont contribué à une réapparition de cette maladie
dans les régions où elle était précédemment contrôlée. Le but de cette mise au point est de
dégager les particularités cliniques, biologiques et radiologiques de la tuberculose péritonéale
et de présenter les moyens de diagnostic et les modalités thérapeutiques. Le diagnostic de
cette maladie est difficile et demeure un défi en raison de sa nature insidieuse, de la variabilité

∗ Corresponding author. BP 12 bureau de poste, Jadida, 3027 Sfax, Tunisia.

E-mail address: ahmedguirat@yahoo.fr (A. Guirat).

0399-8320/$ – see front matter © 2010 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.gcb.2010.07.023
Peritoneal tuberculosis 61

de sa présentation et des limites des examens de diagnostic disponibles. Cette pathologie se

manifeste habituellement par un tableau d’ascite exsudative à prédominance lymphocytaire.
Il existe une panoplie d’examens complémentaires dont la sensibilité et la spécificité sont
variables pour confirmer le diagnostic de tuberculose péritonéale. L’isolement d’une mycobac-
térie par culture du liquide d’ascite ou de la biopsie péritonéale idéalement réalisée par voie
laparoscopique représente l’examen de choix. Le rôle de la PCR, l’adénosine désaminase asc-
itique, l’interféron gamma et le système radiométrique de BACTEC permettent d’améliorer le
rendement diagnostique. Un traitement pendant six mois avec des antituberculeux du groupe
1 de l’OMS est suffisant dans la plupart des cas.
© 2010 Elsevier Masson SAS. Tous droits réservés.

Introduction the peritoneum. An immune response occurs usually and

Described for the first time in 1843 [1], peritoneal tuber-
culosis (PT) is due to the development of Koch’s Bacillus
(KB) in the peritoneum. It is a disease that poses a public
health problem in endemic areas. The PT risks to evolve into
complications such as septicemia, acute intestinal occlu-
sion and infertility in women. The diagnosis of this disease
is a challenge; the absence of specific clinical signs, the
lack of paraclinical tests with high predictive value and the
pauci-bacillary nature of this disease make the diagnosis of
tuberculosis often based on histological study of biopsies of
peritoneum performed ideally by laparoscopy.
Pathogenesis
Pathogenic agent
the evolution is generally towards healing. However, some
bacteria remain quiescent in the peritoneum for months
or years. Several causes may reduce the defenses of the
organism and can cause the reactivation of the bacilli and
their multiplication [5,6];
• by ruptured retroperitoneal and mesenteric lymph, which
nodes into the peritoneal cavity resulting in the formation
of caseous foci partitioned by fibrosis in places adhering to
the intestinal loops. These secondary foci are formed fol-
lowing the ingestion of the bacteria crossing the intestinal
mucosa to the lymph of the peritoneal cavity or following
hematogenous spread as the first mechanism [7—9];
• from lesions in adjacent organs such as intestine or the
fallopian tubes [10—12];
• by direct contamination of the peritoneum in patients
with chronic renal failure under peritoneal dialysis [13].

PT is caused by several species of Gram-positive bacteria

known as Mycobacterium tuberculosis complex (M. tuber-
culosis, M. africanum, M. bovis, M. caprae, M. microti, M.
pinnipedi. . .). They are united in the same unit for genetic
similarities reasons. These bacteria belong to the family of
Mycobacteriacea and the order of Actinomycetales: they are
characterized by a thick wall, which is rich in fat giving them
special dyeing properties and a relative resistance to many
antiseptics (soda, acid, detergent. . .). The mycobacterium
is 2 to 5 microns in length, very sensitive to heat but resis-
tant to cold and desiccation, colored red by the fuchsin, not
discolored by nitric acid or alcohol from where the nomina-
tion of acid-fast bacillus-resistant (AFB). It grows in aerobic
strictly between 35 and 37 C on enriched media including
that of Lowenstein-Jensen [2].
‘‘Atypical’’ mycobacteria are bacteria present in the
environment and usually non-pathogenic, but which may be
responsible for peritoneal mycobacteriosis. Mycobacteruim
avium complex is the most common cause of mycobacterio-
sis in immunosuppressed patients (AIDS) [3,4].
Modes of contamination
Mycobacteria can infect the peritoneum by different mech-
anisms:
• hematogenous spread of bacilli from a primary pulmonary
site of tuberculosis infection to secondary foci such as
Mechanism of ascites formation
In PT, ascites usually results from peritoneal lymphatic
obstruction caused by a blocking of the peritoneal fluid
reabsorption [14]. Rarely, ascites may result from portal
hypertension secondary to portal vein compression by tuber-
culous lymph nodes but the characteristics of ascites are so
different [10,15,16].
Epidemiology
In recent years, there has been an increase in the total
number of new cases of tuberculosis. The World Health Orga-
nization (WHO) has estimated that the number of new cases
of PT disease in 2007 was about 9.27 million. This repre-
sents an increase from 9.24 million cases in 2006, 8.3 million
cases in 2000 and 6.6 million cases in 1990. Most of the esti-
mated cases in 2007 were recorded in Asia (55%) and Africa
(31%), a small proportion of cases in the Eastern Mediter-
ranean Region (6%), the European Region (5%) and Region of
the Americas (3%). Of the 9.27 million new cases in 2007, an
estimated 1.37 million (15%) were suffering from AIDS, 79%
of these patients came from the African Region and 11% of
the Southeast Asia Region [17].
The PT remains a public health problem in endemic areas.
It represents 1% to 2% of all localizations of tuberculosis
[18] and 31% to 58% of abdominal localizations [19—21]. It
62 A. Guirat et al.

is associated with pulmonary tuberculosis in 3.5% of cases

Table 1 Frequency of various clinical signs of peritoneal
[22]. As in pulmonary tuberculosis where the incidence is
tuberculosis according to the literature.
higher among younger subjects between 25 and 44 years
in developing countries [23], the PT is typically observed in Clinical Signs Frequency (%)
young adults between the third or fourth decade [22,24]. For Ascites 35—100
some authors, the average age is even younger than 28 years [29—32,35,38,43,47,95,103]
[25]. A frequency among women was found in most published Abdominal pains 49—100
series. Neither pathogenic nor physiological explanation is [6,27,30,31,35,38,43,47,103]
advanced for this frequency. Isolated fever 52—76.1
[27,29,30,35,38,43,47,50,103,104]
Contributing factors Abdominal distension 62.5—73 [38]
Abdominal tenderness 47.7 [22]
Constipation 7.1—31 [32,35,38—40,44,99]
The factors favoring overall tuberculosis disease are:
Diarrhea 4.7—1.4
[22,29,30,39,40,44,99,103]
• the pandemic infection of acquired immunodeficiency
Hepatomegaly 2.3—8.2
virus [26,27]: about 9% of new cases of PT (31% in Africa)
[22,29,36,40,44,72,94,99,105,106]
had occurred among AIDS patients [25];
Splenomegaly 2.3—4.3
• the prolonged corcticosteroid [28];
[22,29,36,47,94,99,105]
• the low socio-economic conditions of poor living, poor
hygiene and overcrowding. The literature data suggest
that the incidence of the disease is particularly high in
[39,40]. The sedimentation rate is always increased but the
rural areas [22,29];
values do not exceed 60 mm per hour in more than half of
• treatment with TNF␣ (tumor necrosis factor) [30—32].
the cases [39].
Other predisposing factors for the occurrence of PT have
been reported in the literature such as: Analysis of ascetic fluid

• chronic renal failure on peritoneal dialysis [33]; Macroscopic

• the BCG therapy: use in bladder instillation of Bacil-
lus Calmette-Guérin in the treatment and prevention of
recurrent superficial bladder carcinoma has been impli-
cated in outbreaks of PT [34];
• alcoholism and alcoholic cirrhosis [35,36].
The clinical manifestations
PT is a subacute disease and its symptoms often evolve over
a period of several weeks to months. The average consulta-
tion time compared to the first symptom varied between 2
and 4 months [29].
This disease can be manifested by different clinical
forms. The presenting symptoms of PT are unspecific, which
makes the diagnosis a challenge. Some clinical signs are
frequently found in most series, such as ascites (most com-
mon clinical sign), abdominal pain, night sweats, fever and
abdominal distension (Table 1). In most cases, the discovery
of PT is done during the waning of ascites. PT is diagnosed
in 6.6% of the ascites cases [37]. This rate can reach 65.5%
during exploration of exudative ascites in an endemic area
[38].
The diagnostic approaches
Assessment standard blood
The standard blood test abnormalities are non-specific and
therefore they have a low diagnostic value. A mild nor-
mocytic normochromic anemia and thrombocytosis are the
main abnormalities [11,36,39]. The white blood cells rate
is generally normal, however lymphocytosis is often found
In PT, ascites is usually yellow citrine. This characteristic is
found in 77% to 91% of the cases [39,41]. The ascites fluid
may also take a cloudy appearance, chylous or hematic.
Protein content
In PT, the exudative ascites is a quasi-constant [42], usually
with protein content higher than 30 g/l.
Cellularity
The ascites fluid of PT is often rich in cells (> 400 E/ml) with
lymphocyte predominance (> 60%) [22,43]. A recent meta-
analysis that included 39 English sets about PT has found a
lymphocytic predominance in 68.3% of cases [22]. The pre-
dominance of neutrophils is sometimes found especially in
case of concomitant renal failure or in case of infection of
ascites with another common germ [22]. Thus, an exudative
ascites rich in lymphocytic cells is suggestive but not specific
of PT.
Cytological study
Cytological examination of the ascitic fluid must always
be performed to look for neoplastic cells indicating the
existence of carcinomatous ascites, which is the main dif-
ferential diagnosis of PT.
Biochemical of ascitic fluid
The literature review shows that no biochemical marker is
useful for the diagnosis of PT.
LDH essay. Normally the rate of LDH in ascites is less than
half that of serum. In case of tuberculosis, a rate of LDH
greater than 90 IU/l has a sensitivity ranging between 77%
and 90%, but a low specificity (14%) [22].Serum amino-acid
gradient (SAAG)
Peritoneal tuberculosis
This gradient is calculated by measuring the difference
between the concentrations of albumin in serum and in
ascites collected on the same day. It reflects the charac-
teristic of exudative ascites when its value is greater than
11 g/l and portal hypertension when its value is greater
than 11 g/l [44]. This specificity for portal hypertension
is estimated at 97% [45]. A low gradient less than 11 g/l
was found in 100% of tuberculosis patients [43,46,47],
but this sensitivity decreases in patients having an asso-
ciated cirrhosis reaching values ranging from 29% to 88%
[26,43]. Besides specificity, it is low. Indeed, SAAG less
than 11 g/l is also found in patients having carcinomatosis
[43,47,48].
Glucose determination. A low concentration of glucose in
the ascites fluid may be in favor of PT [22,40]. However, data
are insufficient to decide about the value of a systematic
assay.
Thus, assays of LDH, SAAG and glucose have a speci-
ficity too low to be recommended for the diagnosis of
PT.
Microbiological study
Microscopy: search of Mycobacterium tuberculosis (MT).
The microscopic diagnosis on a single smear made from the
crushed uses dye specific property of the wall of mycobac-
teria, which is acid-alcohol resistance. This is a quick
technique that is also accessible. Due to the pauci-bacillary
nature of PT, microscopic examination has a sensitivity of
less than 10% [22,35,38,46,49].
Culture. The isolation of MT in the culture of ascitic fluid
or in cell homogenates of biopsies confirm the diagnosis of
PT.
Solid culture medium. This test requires 10 to 50 ml of
ascites, ultra-centrifuged and then cultured on Lowenstein-
Jensen medium. This method has a sensitivity of around 35%
[35,50]. The major drawback of culture is the time needed
to obtain the result. Indeed, the average time of bacterio-
logical results is 45 days [22], which is not conforming to the
requirements and urgent diagnosis.
Liquid culture medium. The use of automated BACTEC
is a recent method allowing for more rapid detection of
MT in an average of 14 to 27 days [22,35]. It is a radio-
metric system allowing the acceleration of the discovery
of MT by reducing the culture time by half [51]. The
time of bacteriological results is shortened to 15 days but
requires one liter of ascites ultra-centrifuged. This method
has a large positivity rate, which varies from 66% to 83%.
A comparative study of its use, compared to Lowenstein-
Jensen medium on any type of sample showed a higher
sensitivity of detection of MT as atypical mycobacteria
(100% versus 51.7%), a better specificity (94.7% versus
78.9%) and a higher negative predictive value (100% ver-
sus 78.9%) [48]. However, this method is more expensive
than the solid culture medium, and it uses a radioactive
material, which poses a problem of manipulation. To over-
come these drawbacks, other non-radioactive culture media
have been developed with the same advantages of rapid
growth [52]. These environments are used manually (BBL®
tube, MGITTM , MB Redox system) or via automated systems
(BP BACTECTM , 9000MB, BACTECTM MGITTM 960 Bac T/Alert
3DTM ).
63
CA-125 determination
Some authors have found that rates of CA-125 were high
in both serum and ascites in the majority of patients with
exudative ascites whatever the etiology [53,54]. Other stud-
ies have reported high levels of this marker in both serum
and ascites of patients with PT [55,56] and can therefore
be confused with ovarian carcinoma at an advanced stage.
Thus, a high rate of CA-125 should always evoke PT in differ-
ential diagnosis of ovarian carcinoma mainly among women
living in endemic areas. In addition, the finding of a high CA-
125 in ascites rich in proteins in a woman may lead to a false
diagnosis of ovarian cancer and tuberculosis underrate.
Moreover, several studies have noted that under quadru-
ple anti-tubercular drugs, after histological confirmation of
the PT diagnosis, the rate of CA-125 decreased gradually
and returned to normal even after 1 to 2 months on average
[22,53,54,56,57]. Thus, the determination of CA-125 seems
useful for evaluating the therapeutic response of PT. This
feature remains to be confirmed by prospective studies.
The determination of the activity of adenosine
deaminase in ascites (ADA)
Several studies have reported an increase of ADA in some
body fluids in disorders that involve an immune reaction cell
type such as tuberculosis, empyema, rheumatoid arthritis
and malignant lymphomas [58,59].
In PT, the increase of adenosine deaminase may be the
result of activation of T cells in response to mycobacterial
antigens, on the threshold of 30 U/l and in the absence of
immunosuppression or cirrhosis, this test has a sensitivity of
96%, a specificity of 98% (Table 2), positive predictive value
of 95% and a negative predictive value of 98% [22,60,61]. It
is a cheap and reproducible test.
According to the recommendations of the Society of
Pneumology in the French language for the management of
tuberculosis in France published in 2004, the utility of the
peritoneal assay of ADA depends more on economic and epi-
demiological criteria than on its sensitivity or its specificity:
in endemic area where invasive techniques like laparoscopy
are not available or costly, the ADA is helpful. Elsewhere, the
ADA will be useful if positive, it confirms a clinical suspicion
of TB for inoperable patient [62].
In a recent meta-analysis that included four prospective
studies reporting 264 cases of ascites, Riquelme et al. have
shown that for a rate between 36 and 40 IU/L, the ADA has a
sensitivity of 100% and a specificity of 97% for the diagnosis
of PT [63]. The authors concluded that the determination
of the ADA is a rapid and accurate test for the diagnosis
of PT. In case of high rate, the introduction of empirical
antituberculosis treatment is justified while waiting for the
results of mycobacteria culture or biopsy [63].
Immunological tests
Tuberculin skin test (TST)
The TST is testing cell memory response to mycobacterial
antigens. It explores the capacity of memory lympho-
cytes in the patient after stimulation with these antigens,
to secrete cytokines (IFN-gamma especially) responsible
64 A. Guirat et al.

Table 2 Sensitivity, specificity and threshold values of ADA in some studies reported in the literature.

Series Year Number Sensitivity (%) Specificity (%) Value (U/L)

Voigt et al. [107] 1989 41 100 96 112.6
Bhargava et al. [108] 1990 87 100 97 36
Ribera et al. [109] 1991 86 100 97 40
Soliman et al. [110] 1994 50 94.4 100 28
Sathar et al. [68] 1995 93 96 96 30
Brant et al. [111] 1995 44 100 92 31
Burgess et al. [60] 2001 178 94 92 30
El Abkari et al. [24] 2006 123 96 98 —
Riquelme et al. [63] 2006 264 100 97 39
Sharma et al. [112] 2006 119 97 94 58
Dewivedi [113] 2008 49 100 96.6 33

for induration at the injection site, if the subject is
ill [64].
The positivity of the TST is not specific for active tubercu-
losis, but merely reflects an awareness by prior contact with
the MT. Its interpretation varies depending on the immune
status of patients, history of vaccination, contagion or pri-
mary infection. Similarly, the sensitivity of this test is low;
false negatives are reported in 15% to 60% in the literature
[65,66].
Gene amplification by ligase chain reaction (LCR)
It is a molecular amplification test recently introduced into
medical practice. According to Gamboa et al. [73], this
method has a sensitivity of 77.7%, specificity of 98.7% and a
negative predictive value of 95.2% for the diagnosis of extra
pulmonary tuberculosis; its diagnostic effectiveness is then
significantly higher than that of PCR. Unfortunately, this test
is still very expensive and therefore difficult to insert in
practice especially in endemic countries.

Determination of gamma interferon Radiological explorations

It is a quantitative test that assesses the cell-mediated
immune response against MT. It is based on the fact that
T cells secreting gamma interferon were necessarily aware
in advance [22]. This assay has a sensitivity of 89% for the
diagnosis of latent forms of PT [67]. Some authors advocate
the measurement of gamma interferon coupled with that
of adenosine deaminase, thereby increasing their respec-
tive sensitivity and specificity for the positive diagnosis of
tuberculosis [68]. According to Sathar et al. [68], the gamma
interferon assay has a sensitivity of 93% and a specificity of
98% when the rate was 3.2 IU/ml, the sensitivity of adeno-
sine deaminase is 93% and its specificity is 96%, when the
rate is 30 IU/l. Unfortunately this is not a common practice
test. Thus, the dosage of interferon gamma may be an alter-
native diagnosis compared to surgery in countries with high
endemic TB.
Determination of specific immunoglobulin
A recent review on the immunological diagnosis of tuber-
culosis has shown that the determination of IgG antibody
response to 43-kDa antigen of MT in ascites had a high sen-
sitivity approaching 100% and a specificity of 95.7% [69]. It
is a very expensive test performed in specialized centers.
Abdominal ultrasounds
Abdominal ultrasound can evoke some signs in favor of PT
but cannot confirm diagnosis [74], and can follow the evo-
lution under treatment. The ascites is the most frequent
ultrasound sign (45% to 100% of cases) [75,76]. It is free in
most cases and appears as trans-sonic images in which the
bowel loops float. Ascites may take echogenicity related to
its exudative nature [77]. Sometimes, the ascites is par-
titioned, which is an argument in favor of its tubercular
origin and could predict technical difficulties during diag-
nostic laparoscopy. Other signs suggestive of PT can be
highlighted, such as the thickening of the peritoneum, the
clumping of bowel loops side by side each other or to the
anterior abdominal wall [78], peritoneal nodules that are the
equivalent of granulations sitting at the visceral and parietal
peritoneum [75,78,79], adhesions visualized as hypoechoic
linear structures in thin strips and floating in the tuberculosis
peritoneal effusion [78,80], and the deep lymph nodes often
described as hypoechoic multiple masses and sometimes
confluent [75,76,80]. All these echographic signs taken sep-
arately have no diagnostic value in the PT. On the contrary,
their association should suggest the diagnosis [75]. How-
ever, the problem of differential diagnosis with peritoneal
carcinomatosis remains.

The molecular genetics

Testing the polymerase chain reaction (PCR)
The reaction of gene amplification by PCR is a rapid test
to isolate the MT between 24 to 48 hours [70]. The use in
clinical practice of this technique is limited by high cost and
low sensitivity (60% to 80%) [71,72].
Computed tomography (CT)
This examination is often done through the assessment of
exploration of exudative ascites isolated in order to find a
primary tumor such as advanced ovarian cancer, the main
differential diagnosis of PT [56,81].
The major CT signs suggestive of PT are:
Peritoneal tuberculosis
Figure 1 Free high-density ascites with thickening of the pari-
etal peritoneum (arrow).
• the ascites, which typically has a high density (25 to 45
HU) [82,83], but at an early stage it may have a fluid
density [84,85] (Fig. 1);
• lymph nodes, which usually have hypodense center [84]
corresponding to the caseating with hyperdense rim but
can also be calcified [86];
• thickening of the mesentery and omentum [87—89];
• regular and uniform thickening of the peritoneum [84,89]
(Fig. 1);
• agglutination of the intestinal loops [85,89].
The surgical biopsies
Surgical approach
They remain the ultimate means to confirm the diagnosis
of PT-related histological proof. These biopsies are typ-
ically done by laparotomy or in recent years ideally by
laparoscopy. They must interest the peritoneum zones,
which contain nodular lesions. The feasibility of laparoscopy
in the exploration of ascites is well established [90—93].
Cumulative data from 402 patients in 11 studies, reported
at a recent systematic review, showed rates of sensitivity
and specificity of 93% and 98% respectively [22]. In addition,
laparoscopy is a surgical approach that gives less parietal
prejudice and less postoperative pain than laparotomy. It
also allows the reduction of hospital stay and quicker reha-
bilitation.
The complications rate of laparoscopy biopsies is around
2.7%; the most common are intestinal perforations and
bleeding from wounds of large vessels [11,93] especially
in the fibro-adhesive forms [24]. Therefore the diagnostic
laparoscopy in case of exudative ascites should be entrusted
to an experienced surgeon.
Macroscopic findings
The macroscopic appearance of PT is typical when we find
regular white granules with equivalent sizes (1 to 3 mm),
numerous nodules, dispersed and friable at biopsy, hyper-
emia of the peritoneum, filamentous (or rope) peritoneal
adhesions and clumping of bowel loops with fibrin deposition
[94].
65
Figure 2 Tuberculous granuloma consisting in giant cells of
Langhans-type, epithelioid cells, histiocytes and eosinophils.
However, face to atypical macroscopic PT, we should
always evoke the peritoneal carcinomatosis, which typi-
cally includes peritoneal nodules of varying sizes, irregular,
inverted, retractable, preferably located on the diaphragm
and/or in the pelvis with a non-inflammatory peritoneum.
The pathological study of biopsies
Histologically, typical lesions of tuberculosis is represented
by the tuber, which corresponds to caseating epithe-
lioid granuloma containing multi-nucleated giant cells
‘‘Langhans-type’’, epithelioid histiocytes and lymphocytes
forming a ring surrounding a central area of caseous necrosis
(Fig. 2).
Percutaneous biopsy
Liver biopsy
A granulomatous liver disease may be associated with peri-
toneal involvement in varying proportions ranging from 25%
to 48% [38,72,95]. For some authors, liver biopsy must be
systematic face to any suspicion of PT, it would provide,
in some cases, the only evidence of tuberculous etiology
without resorting to invasive procedures [96].
Peritoneal biopsies
This is a new minimally invasive method with little or no
complications and could allow to obtain very good results.
Vardareli et al. [47] reported 19 cases of PT with ascites
(fibro-adhesive forms excluded) of which 18 were diag-
nosed by peritoneal biopsy under percutaneous radiological
guidance. Thus, this method could avoid the drawbacks
of surgery, and preliminary results seem very encouraging.
Studies on a larger scale trials will help to confirm the contri-
bution of this new diagnostic procedure.
Treatment
The treatment of PT is medical. The delay in initiating treat-
ment may increase mortality. Chow et al. [35] reported a
significant deterioration in clinical status of over 80% of
66
patients during the exploration period. The overall mortality
in this study was 35%, whereas in the subgroup of patients
with underlying cirrhosis mortality reached 73%. The aver-
age mortality rate according to the cumulative data from
18 studies, which included more than 800 patients was 19%
[14]. This underlines the importance of establishing appro-
priate treatment as soon as possible.
The antituberculosis drugs were classified into first and
second line. Currently, WHO has divided them into five
groups. The first-line drugs are a group 1 of WHO: isoniazid
(INH), rifampicin (RIF), pyrazinamide (PZA), ethambutol
(EMB). Those of second-line bring together groups 2 to 5
of the WHO [97].
The currently recommended protocol combines four
drugs INH, RIF, PZA and EMB given daily for 2 months,
relayed by 4 months of combination therapy INH and RIF
[98]. Although the recommended duration of treatment of
PT is 6 months, some authors have reported treatment dura-
tion to 12 months [29]. There is however no evidence to
hold a treatment time beyond 6 months. Some retrospec-
tive series have used different regimens of 6 or 9 months,
and found that the majority of their patients has responded
to treatment similarly [43,47]. One study compared two dif-
ferent durations of treatment (9 months and more than 12
months) and found no significant difference in terms of ther-
apeutic response in either group [99].
The favorable response to treatment results in the res-
olution of symptoms and the disappearance of ascites.
Laboratory abnormalities in favor of disease activity will usu-
ally normalize within 3 months after starting the treatment
[22].
The risk of hepatotoxicity of antituberculosis drug
increases in case of underlying liver disease and particu-
larly cirrhosis. Stopping the treatment is recommended in
cases of elevated transaminases up to five times normal in
asymptomatic forms, and three times normal in case of signs
of hepatotoxicity [98]. In this case it is important to choose
one of four alternatives:
• RIF, PZA and EMB during 6 months;
• INH, RIF, EMB during 2 months followed by INH and RIF
during 7 months;
• RIF, EMB, fluoroquinolone, and cycloserine (injection) dur-
ing 12 to 18 months;
• EMB, streptomycin, fluoroquinolones and other second-
line anti-TB drugs.
In the serie of Sanai and Bzeizi [22], no cases of hepa-
totoxicity have been reported in 16 patients who had liver
disease and treated with INH, RIF, EMB and ofloxacin during
2 months followed by INH and EMB and ofloxacin during 10
months.
The use of corticosteroids is still controversial. Some
authors have shown no benefit in combining corticosteroids
with antituberculosis [100] while others have found the
opposite [101,102]. Prospective studies are needed to better
understand the contribution of corticosteroids.
Conclusion
PT remains a common public health problem in endemic
regions of the world. The diagnosis of this disease is difficult
A. Guirat et al.
because of its clinical polymorphism. Assays of LDH, SAAG
and glucose have a specificity that is too low. PCR tests
are expensive and have low sensitivity. The research of MT
in the ascites fluid is insensitive; culture in liquid media
such as BACTEC radiometric system improves the diagnos-
tic sensitivity in a reasonable timeframe. The dosage of
the ADA is a quick test, reproducible with excellent sen-
sitivity and specificity for the diagnosis of PT. It should
be used routinely in endemic countries. It is the same for
gamma interferon, which has a very high sensitivity and
specificity. The determination of CA-125 would allow the
assessment of therapeutic response. The ideal peritoneal
biopsies performed by laparoscopy can confirm the diag-
nosis while avoiding the disadvantages of laparotomy. The
interventional radiology seems promising for the realization
of peritoneal biopsies. Treatment involves antituberculosis
drug of group 1 according to the WHO during 6 months.
Conflict of interest statement
The authors have not declared any conflict of interest.
Acknowledgments
The authors would like to thank Pr Ben Amar
Mohamed (benammed@yahoo.fr) and Mrs Ahlem Fendri
(ahlem fendri@yahoo.fr) for their precious help in the
translation of the manuscript and for her constant support.
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