Access to this full-text is provided by Wiley.
Content available from Case Reports in Medicine
This content is subject to copyright. Terms and conditions apply.
Case Report
Gastrointestinal CMV Disease and Tuberculosis in an
AIDS Patient: Synergistic Interaction between
Opportunistic Coinfections
Miriã Boaretto Teixeira Fernandes , Pedro Afonso Nogueira Mois´
es Cardoso,
Luiza Bassani Alto´
e, Izana Junqueira de Castro, Guilherme Almeida Rosa da Silva ,
Walter de Ara ´
ujo Eyer-Silva , Marcia Lyrio Sindorf, Rodrigo Panno Bas´
ılio de Oliveira,
Marcelo Costa Velho Mendes de Azevedo, and Jorge Francisco da Cunha Pinto
Universidade Federal do Estado do Rio de Janeiro (UNIRIO), Rio de Janeiro, RJ, Brazil
Correspondence should be addressed to Miriã Boaretto Teixeira Fernandes; mi.boaretto@gmail.com
Received 27 January 2018; Revised 11 April 2018; Accepted 8 May 2018; Published 11 June 2018
Academic Editor: Stephen A. Klotz
Copyright ©2018 Miriã Boaretto Teixeira Fernandes et al. is is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
e AIDS pandemic has made diseases such as tuberculosis, CMV disease, and other opportunistic infections more prevalent;
these diseases may even be found to be associated among themselves, and the natural history of each disease may present in an
unusual manner. We report the case of a 41-year-old man with HIV (CD4 of 144 cells/dL) and HCV with hematochezia due to
tuberculosis in the ileocecal valve and descending colon and CMV tissue invasive disease in the esophagus and descending colon.
Coinfection among tuberculosis and cytomegalovirus in the gastrointestinal tract was described only once in a patient with
a recent diagnosis of HIV that aected the distal ileum and ascending colon. We will discuss the peculiarities of the case and the
behavior of the immune system in the face of simultaneous opportunistic infections. is is a challenging scenario that has scarce
publications and is of great clinical importance.
1. Introduction
e pandemic human immunodeciency virus (HIV) has
dramatically changed the opportunistic infections epide-
miology, such as for tuberculosis and cytomegalovirus
(CMV) disease. Both have become more prevalent and could
be found in association in the same patient, possibly with an
unusual natural history [1–4]. e neglect and poor adhesion
to antiretroviral therapy (ART), the therapeutic failure, and
the lack of access to this therapy made possible that this type
of manifestation continued to occur in the same manner it
used to occur in the pre-ART era [1–4].
e highest prevalence of tuberculosis cases is concen-
trated in the south of Asia and Africa [5]. However, in Brazil,
mostly in Rio de Janeiro, the Brazilian province with highest
prevalence, the disease’s incidence is approximately 70.57 in
100,000 inhabitants in 2012 [6]. e low socioeconomic
condition, undiagnosed sick people in circulation, and the
poor adherence to treatment result in an increase of new
cases, which are often associated with HIV immunode-
pression [7]. It is estimated that 95% of the cases in the world
occur in underdeveloped or emerging countries with lower
life quality, which shows the relationship between this
disease and socioeconomic issues [8]. By 2015, it was esti-
mated that at least 11 million people were coinfected with
HIV and Mycobacterium tuberculosis in the world, and from
individuals diagnosed with tuberculosis in 2007, approxi-
mately 11% were HIV positive. Tuberculosis in the gas-
trointestinal tract, of interest to our case, is a less common
presentation compared to the classical pulmonary form,
which occurs mainly in immunosuppressed individuals [9].
Another infectious agent of interest to our study, which
became more prevalent with the spread of AIDS, is cyto-
megalovirus (CMV), a virus from the herpesvirus family.
Hindawi
Case Reports in Medicine
Volume 2018, Article ID 8047892, 7 pages
https://doi.org/10.1155/2018/8047892
Beyond the congenital, the perinatal, and the mononucleosis-
like manifestations, cytomegalovirus is also a typically op-
portunistic infection. In South America, Africa, and Asia,
where the prevalence of CMV infection is higher, primary
infection usually occurs during childhood, following a period
of clinical latency [10]. Reactivation occurs in an immuno-
suppressive situation. CMV promotes vasculitis and in-
ammatory lesions in several tissues, such as the retina, lung,
and gastrointestinal tract, especially in HIV patients with CD4
T cells <50 cells/dL [11, 12].
A relevant topic is that the simultaneous manifestations
of opportunistic diseases in the context of AIDS are re-
current, reaching up to 33% of the patients who have some
opportunistic presentation [13]. is fact creates a chal-
lenging condition due to the dicult diagnosis because
physicians are trained to diagnose parsimoniously, and
multiple infections of the same anatomical site can simulate
a single infection due to the similarity of the symptoms
among them [14, 15]. Regarding the possible synergisms in
the coinfection by dierent agents, bidirectional interaction
of HIV and tuberculosis coinfection has already been de-
scribed, such that one contributes to the aggravation of the
other. HIV increases the risk of reinfection and reactivation
of M. tuberculosis by reducing the 1 response prole of the
immune system. At the same time, tuberculosis in the pa-
tient with HIV promotes a reduction of CD4+ T cells and
accelerates HIV replication through the production of tumor
necrosis factor-alpha (TNF-alpha) and monocyte chemo-
tactic protein 1 (MCP1) [14, 16].
We will discuss the correlation and immunological eects
of HIV, M. tuberculosis, and CMV coinfection by reporting
a case of tuberculosis in the ileocecal valve and descending
colon and cytomegalovirus in the esophagus and descending
colon, as well as with chronic hepatitis C virus (HCV) in-
fection. e understanding of the behavior of the immune
system in the face of simultaneous infections is a challenging
scenario with scarce publications, especially about humoral
and cellular immune response aspects.
2. Case Report
A 41-year-old man, a native from Rio de Janeiro and an HIV
and HCV carrier, without criteria for the treatment for HCV
(detectable viral load, without cirrhosis and with normal
transaminase levels), who had abandoned ART, had attended
the Gare´
eand Guinle University Hospital’s immunology
clinic complaining about continuous epigastric burning pain
without irradiation and with diuse abdominal pain that was
mild and continuous, which had started approximately two
months prior to admission. He also complained about intense
hematochezia that had started three weeks before, with in-
tense ow and with “pure blood” appearance without clots.
He presented with daily hyperthermia since the abdominal
symptoms had started with intermittent high fever and an
over 10% body weight loss in the same period. e physical
examination revealed oral candidiasis, bleached mucous
membranes, and cachexia. At the admission time, the HIV
viral load was recorded at 905,569 copies per ml, and the
TCD4 lymphocyte count was 144 cells/dL. Prophylactic
sulfamethoxazole-trimethoprim 400/80 mg 2 IV ampoules
once daily and uconazole 200 mg IV once daily for treatment
of the oral candidiasis were prescribed. e patient’s con-
dition evolved without major occurrences or complaints,
presented with high fever, above 38°C almost every day. Blood
counts revealed thrombocytopenia, neutrophilia, lympho-
penia, anemia, microcytosis, and anisocytosis (Table 1). e
medical team requested upper digestive endoscopy (Figure 1)
and colonoscopy (Figure 2), which veried the presence of
ulcer with irregular and raised edges, brinonecrotic base,
measuring approximately 3 cm in the middle third of the
esophagus and 30 cm from the incisors and the mild antrum
gastritis, and swollen, irregular, and brinous ulcers in the
ileocecal valve, descending colon, and all other segments. e
lesions were similar to those found in the esophagus, which
could suggest the same etiology. It was suggested by the
internal medicine team that the diagnosis could be a coin-
fection (tuberculosis, cytomegalovirus, and herpes simplex
virus disease). e diagnosis of tuberculosis and cytomega-
lovirus coinfection of the gastrointestinal tract was conrmed
by the histopathological report (Ziehl–Neelsen staining of
acid-fast bacilli, CMV intracytoplasmic inclusions in Giemsa
staining, and immunohistochemical study with positive la-
beling for CMV in cells with clear halos), and some time later,
culture with the growth of M. tuberculosis (Figure 3).
Treatment was started with an RIPE scheme (rifampicin
+ isoniazid + pyrazinamide + ethambutol) 4 tablets daily and
ganciclovir 350 mg IV for 21 days with a weight gain of 4 kg
and clinical and laboratory improvement. He was discharged
from the hospital with ART lamivudine, tenofovir, and efa-
virenz (TDF + 3TC+ EFV) one tablet per day and was re-
ferred to a clinical follow-up for tuberculosis and HIV/HCV
coinfection monitoring. At the end of the treatment for tu-
berculosis and 6 months after ART was restarted, the patient’s
viral load was <40 copies/dL and the CD4+ T-cell count was
356 cells/dL, asymptomatic.
3. Discussion
In the present case, an AIDS patient with ART abandon,
coinfected with HCV, tuberculosis, and simultaneous cy-
tomegalovirus in the gastrointestinal tract, was reported. In
Table 1: Blood count on admission.
White blood cells
(dierential) 6.4 (10/μL) (0/0/0/0/11/65/15/9) (%)
Red blood cells 4.3 (10/μL)
Hemoglobin 10.8 (10/μL)
Hematocrit 33.3 (%)
MCV 77.4 (fL)
MCH 25.1 (pg)
MCHC 32.4 (g/dL)
Platelets 71 (10/μL)
RDW-SD 43.3 (fL)
RDW-CV 16.4 (%)
MPV — (fL)
Neutrophils 6.18 (10/μL), 73.5%
Lymphocytes 1.5 (10/μL), 17.9%
2Case Reports in Medicine
the laboratory tests, microcytic anemia with anisocytosis
suggested iron deciency secondary to nutritional causes
and chronic gastrointestinal bleeding. AIDS-typical labo-
ratory ndings were lymphopenia with neutrophilia and
thrombocytopenia, which may also be related to chronic
HCV infection [17].
CMV retinitis is the most frequent presentation of
cytomegalovirus, accounting for up to two-thirds of the
manifestations in target organs [18]. However, it is not
uncommon to nd extraocular manifestations in immu-
nosuppressed patients, such as the pulmonary, neurological,
and intestinal forms; the last one represents approximately 5
to 10% of the total [11, 18]. In gastrointestinal cytomega-
lovirus, colitis is the most common presentation, followed
by esophagitis [19], occurring exactly at these sites in the
case described. In tuberculosis cases, the most frequent
form is pulmonary, and the extrapulmonary forms, less
common and related to immunosuppression, represent only
14.4% of all diagnoses [1, 7]. From all the extrapulmonary
forms, the intestinal is the sixth in frequency, and ap-
proximately 25–30% of the cases have the concomitant
pulmonary form, which was not observed in our patient.
e esophageal involvement here presented is rare and of
lesser severity, representing only 0.15% of all deaths due to
tuberculosis [9].
e tuberculosis and cytomegalovirus coinfection, al-
though rarely described, has been already reported in other
tissues [4, 20, 21]. In the gastrointestinal tract, it was de-
scribed only once, in a patient with a recent diagnosis of
HIV, aecting the distal ileum and ascending colon, pre-
senting shock due to massive intestinal hemorrhage. As such
complications are rare in intestinal tuberculosis, the hy-
pothesis was raised that this complication could have been
caused by a possible synergism between tuberculosis and
cytomegalovirus, which was conrmed by histopathology
[3]. However, the esophagus involvement by these two
diseases together, as in the case here presented, has not been
described yet.
e negative eect that HIV infection plays on the
TH1 immune response prole, which is the main eective
response against mycobacteria [16] and essential for
maintaining CMV latency [4], is a determining immu-
nological factor for this type of association [16]. Addi-
tionally, the cytopathic lesion that HIV itself produces in
the intestinal epithelium is already a facilitator to new
infections in this site [22]. is process occurs by the virus
direct toxic action, by the lymphocytes inammatory
inltrate in the lamina propria, and by the gastrointestinal
immune system activation, with increased TNF-alpha
production, a cytokine related to enterocytes apoptosis
Figure 1: Upper digestive endoscopy showing an irregular ulcer with raised edges, brinolytic background, measuring approximately 3 cm
in the middle third of the esophagus and 30 cm from the incisors and mild antrum gastritis.
Case Reports in Medicine 3
[23]. On the other hand, what we have observed is that the
opportunistic infections themselves also contribute to the
HIV progression. As HIV is predisposed to infect CD4+
T cells, any local infection that causes the recruitment of
such cells will lead to more infection targets for the virus
and its consequent replication [23]. Tuberculosis infec-
tion also promotes the abrupt decline in CD4+ T cells in
HIV carriers, more specically the 1 cells. Additionally,
increased viral replication has been demonstrated in those
macrophages located in mycobacterial-infected sites, due
to the increase of NF-kappa beta and TNF-alpha [15, 16].
Moreover, the relative risk of death and development of
other opportunistic infections is greater in patients with
HIV-TB coinfection [24].
Tuberculosis has also been demonstrated to inuence
CMV reactivation by inducing Mip-1beta production by
CMV-specic response CD4 cells. us, tuberculosis in-
fection also becomes a risk factor for CMV reactivation by
accelerating the immunodepression progression by HIV. In
addition, tuberculosis also stimulates the production of
inammatory cytokines that aid CMV reactivation [4].
As tuberculosis is an infection that manifests itself in-
dependently of CD4 T-cell levels [14], it is more likely to be
the rst opportunistic infection to occur and thus predispose
the organism to others that occur with a lower CD4 count,
such as CMV. However, as in the case described, the pre-
sentation of tuberculosis was intestinal, which depends on
a more pronounced immunosuppression degree, and further
without concomitant pulmonary infection, we cannot rule
out the hypothesis that CMV would have appeared initially
and, by the local replication of HIV itself, it would have
caused tuberculosis reactivation at the same site.
Additionally, CMV actively infects monocytes, which are
essential cells in the production of inammatory cytokines
that modulate the immune response to tuberculosis and HIV
infection [11, 15]. It is therefore likely that CMV infection
takes part in causing other infections or the reactivation of
opportunistic agents due to inammatory cytokine pro-
duction, similar to what has already been described in tu-
berculosis and HIV. CMV also promotes a change in natural
killer (NK) cell receptor patterns in the body with the
predominance of the inhibitory-type NK cell receptors
(NKG2C) compared to the activation type (NKG2A) [25],
impairing the body’s responses to other agents. e
mechanisms described may partially explain the multidi-
rectional interaction between these infections, so that only
one of them itself is enough to cause the emergence of the
others.
In the other case described in the literature [3], no clinical
improvements were identied until CMV infection was
identied and treated, which necessitates the skilled diagnosis
of coinfections. Table 2 compares clinical and epidemiological
aspects between tuberculosis and CMV infection in the
gastrointestinal tract, demonstrating their main dierences
[9, 16, 26, 27]. e lesions’ appearances, found in our case’s
colonoscopy, were suggestive of ulcerative-type intestinal
Figure 2: Colonoscopy showing ulcers with raised and irregular borders and necrotic background measuring between 1.5 and 2 cm and at
erosions.
4Case Reports in Medicine
tuberculosis, but the signicant ulceration extension that was
found led to the suspicion of a coinfection responsible for
magnifying the damage to the epithelium.
It should be noted that CMV has been reported in AIDS
patients in coinfection with other diseases, such as pneu-
mocystosis and Mycobacterium avium infection in the
pulmonary tract [20, 21], and it has also been proposed as
a facilitating agent for Kaposi’s sarcoma [28]. Likewise,
tuberculosis has been reported in coinfection with other
opportunistic diseases, mainly in the pulmonary tract, such
as pneumocystosis, histoplasmosis, M. avium, and para-
coccidioidomycosis [2, 20, 21, 29, 30]. Possibly, the fre-
quency of these coinfections mentioned above is greater than
we imagine, especially in cases in which presentation occurs
(a) (b)
(c) (d)
(e) (f)
Figure 3: Esophagus (a, d), ileocecal valve (b, e), and colon (c, f). Histopathological examination showing chronic granulomatous in-
ammation with necrotic area and giant cells, at 200x magnication (a, b, and c), in addition to alcohol-acid-resistant bacilli by
Ziehl–Neelsen staining, at 400x magnication (e). (d, f) e immunohistochemical study with positive labeling for CMV in cells with clear
halos, at 400x magnication.
Case Reports in Medicine 5
more severely than usual, with complications such as per-
foration, intestinal obstruction, or major hematochezia.
ese more severe presentations may indicate more than
one agent in a synergistic interaction [3].
us, tuberculosis infection in the esophagus, a non-
prevalent site for this infection, could have resulted from
synergism with CMV causing an infection in a less probable
site with increased ulceration. e hypothesis of coinfections
is valid in less frequent and more aggressive presentations of
opportunistic diseases.
Conflicts of Interest
e authors declare that there are no conicts of interest
regarding the publication of this paper.
References
[1] P. Stride, M. Stare, L. Kelly, R. Horvath, T. Wood, and
C. Alexander, “A rare case of chronic benign tracheo-
oesophageal stula, with Candida albicans cultured from
a pleural eusion,” Journal of the Royal College of Physicians of
Edinburgh, vol. 42, no. 4, pp. 322–324, 2011.
[2] S. Patel, V. J. Abraham, R. M. Mathur, S. Devgarha, and
A. Yadav, “Acquired spontaneous bronchoesophageal stula
in an adult,” Egyptian Journal of Chest Diseases and Tuber-
culosis, vol. 64, no. 1, pp. 209–211, 2015.
[3] R. Baijal, P. K. H. Ramegowda, M. Jain, D. Gupta, N. Shah,
and S. Kulkarni, “Clinical prole and management of tu-
berculous bronchoesophageal stula,” Journal of Digestive
Endoscopy, vol. 4, no. 4, pp. 103–106, 2013.
[4] D. Madi, B. Achappa, J. T. Ramapuram, N. Chowta, and
S. Mahalingaman, “An interesting case of dysphagia in a HIV
patient,” Journal of Clinical and Diagnostic Research, vol. 7,
no. 3, pp. 534–536, 2013.
[5] F. L. Lado, A. G. Gomez, A. C. O. Barr´
on, and J. A. Lopez,
“Bronchoesophageal stulae secondary to tuberculosis,”
Respiration, vol. 69, no. 4, pp. 362–365, 2002.
[6] S. K. Nanaware, D. Gothi, and J. M. Joshi, “Tuberculous
broncho-esophageal stula managed conservatively,” Lung
India, vol. 22, no. 2, p. 65, 2005.
[7] R. Diddee and I. H. Shaw, “Acquired tracheo-oesophageal
stula in adults,” Continuing Education in Anaesthesia Critical
Care & Pain, vol. 6, no. 3, pp. 105–108, 2006.
[8] S. Alkhuja and A. Miller, “Tuberculous bronchoesophageal
stulae in patients infected with the human immunode-
ciency virus: a case report and review,” Heart & Lung: e
Journal of Acute and Critical Care, vol. 27, no. 2, pp. 143–145,
1998.
[9] S. S. Jain, P. O. Somani, R. C. Mahey, D. K. Shah,
Q. Q. Contractor, and P. M. Rathi, “Esophageal tuberculosis
presenting with hematemesis,” World Journal of Gastroin-
testinal Endoscopy, vol. 5, no. 11, p. 581, 2013.
[10] H. C. Devarbhavi, J. F. Alvares, and M. Radhikadevi,
“Esophageal tuberculosis associated with esophagotracheal or
esophagomediastinal stula: report of 10 cases,” Gastroin-
testinal Endoscopy, vol. 57, no. 4, pp. 588–592, 2003.
[11] C. R. Frison, V. Amado, R. T. Rodrigues, and L. S. Caetano,
“F´
ıstula broncoesof´agica em portador de SIDA: relato de
caso,” Jornal Brasileiro De Pneumologia, vol. 24, no. 6,
pp. 371–374, 1998.
[12] P. Goussard and S. Andronikou, “Tuberculous broncho-
oesophageal stula: images demonstrating the pathogene-
sis,” Pediatric Radiology, vol. 40, no. 1, p. 78, 2010.
[13] G. A. Nari, C. G. Huerta, R. B. Revelez, and A. S. Gonz´
alez,
“F´
ıstula es´
ofago-pleural espont´
anea secundaria a candidiasis
en paciente con infecci´
on por el virus de la inmunodeciencia
humana. Una rara complicaci´on de la moniliasis esof´agica,”
Acta Gastroenterologica Latinoamericana, vol. 40, no. 1,
pp. 65–67, 2010.
[14] D. Frager, J. Baer, and D. P. Kotler, “Idiopathic esophageal
ulceration in the acquired immunodeciency syndrome: ra-
diologic reappraisal in 10 patients,” Abdominal Imaging,
vol. 19, no. 1, pp. 2–5, 1994.
[15] L. M. Felmly, W. F. DeNino, and C. E. Denlinger, “Recurrent
esophagopericardial stula in a patient with human immu-
nodeciency virus,” Journal of oracic and Cardiovascular
Surgery, vol. 147, no. 4, pp. e48–e49, 2014.
[16] A. Ankouane, M. Olinga, H. Hadja, R. Djapa, and
N. Ndjitoyap, “Tracheo-oesophageal stula in highly active
antiretroviral therapy patient with AIDS,” OA Case Reports,
vol. 2, no. 11, p. 103, 2013.
[17] J. Lau-Deza and G. Eiger, “Giant HIV-associated esophageal
ulcer causing tracheoesophageal stula and respiratory fail-
ure,” American Journal of Respiratory and Critical Care
Medicine, vol. 187, p. A2764, 2013.
[18] R. De Silva, P. M. Stoopack, and J. P. Raufman, “Esophageal
stulas associated with mycobacterial infection in patients at
risk for AIDS,” Radiology, vol. 175, no. 2, pp. 449–453, 1990.
[19] D. F. Garc´
ıa, E. Baños, A. Hern´
andez-Albujar et al., “Idio-
pathic esophageal ulcer with stulization to the bronchial tree
in a HIV-positive patient,” Revista Española de Enfermedades
Digestivas, vol. 88, no. 2, pp. 133–136, 1996.
[20] J. G. Sainz and R. A. T. Garc´
ıa, “F´
ıstula esof´
agica por tu-
berculosis en un paciente VIH positivo. Reporte de un caso y
revisi´
on bibliogr´
aca,” Medicina Interna de M´
exico, vol. 25,
no. 5, pp. 395–398, 2009.
[21] C. V. Vartian and E. J. Septimus, “Bronchoesophageal stula
due to Mycobacterium tuberculosis and cytomegalovirus in
a patient with AIDS,” Clinical Infectious Diseases, vol. 22,
no. 3, p. 581, 1996.
[22] N. W. Cirillo, D. T. Lyon, and A. M. Schuller, “Trache-
oesophageal stula complicating herpes esophagitis in
AIDS,” American Journal of Gastroenterology, vol. 88, no. 4,
pp. 587–589, 1993.
Table 2: Main dierences between intestinal cytomegalovirus and
intestinal tuberculosis.
Intestinal CMV Intestinal
tuberculosis
Lesion’s features
Large and solitary
ulcer or multiple
ulcers, erosions, and
mucosal hemorrhage
Solitary ulcer with
an excavating base
and rolled-up
nodular edges
Main distribution in
the gastrointestinal
tract
Colon Ileocecal valve
Gender No predilection
for gender Male
Infection prevalence
in HIV patients 3–5% 37%
Relation to
immunosuppression
degree
TCD4 <50 cells/dL Any TCD4
cell counts
Main geographic
distribution
South America, Asia,
and Africa
South America,
Asia, and Africa
6Case Reports in Medicine
[23] S. M. Pastores, D. P. Naidich, C. P. Aranda, G. McGuinnes,
and W. N. Rom, “Intrathoracic adenopathy associated with
pulmonary tuberculosis in patients with human immuno-
deciency virus infection,” Chest, vol. 103, no. 5, pp. 1433–
1437, 1993.
[24] P. Rosario, J. Song, W. Wittenborn, and F. Christian, “Tra-
cheoesophageal stula in AIDS: stent versus primary repair,”
AIDS Patient Care and STDs, vol. 10, no. 6, pp. 334-335, 1996.
[25] M. Ravera, “Tuberculous bronchoesophageal stula in a pa-
tient infected with the HIV virus,” Endoscopy, vol. 29, no. 2,
p. 146, 1997.
[26] F. M. Wigley, H. W. Murray, R. B. Mann, G. P. Saba,
H. Kashima, and J. J. Mann, “Unusual manifestation of tu-
berculosis: TE stula,” American Journal of Medicine, vol. 60,
no. 2, pp. 310–314, 1976.
[27] F. Dronda, I. Fern´
andez-Mart´
ın, A. Gonz´
alez-L´
opez, and
L. Puente, “Delayed development of tuberculous bronchoe-
sophageal stulas in a patient with AIDS necessitates endo-
scopic surgery,” Clinical Infectious Diseases, vol. 21, no. 4,
pp. 1062-1063, 1995.
[28] G. Deshpande, I. Samarasam, S. Banerjee, R. B. Gnanamuthu,
S. Chandran, and G. Mathew, “Benign esophagorespiratory
stula: a case series and a novel technique of denitive
management,” Diseases of the Esophagus, vol. 26, no. 2,
pp. 141–147, 2013.
[29] L. L. Bergier, R. De Souza Pina, R. D. Gl´
oria et al., “F´
ıstula
traqueoesof´agica por tuberculose em paciente com aids:
tratamento conservador por gastrostomia sem uso de med-
icação parenteral,” Cadernos Brasileiros de Medicina, vol. 27,
no. 3, 2015.
[30] G. Pagano, F. Dodi, M. Camera, G. Passalacqua, E. Malfatto,
and A. De Maria, “Tubercular tracheoesophageal stulas in
AIDS patients: primary repair and no surgery required?,”
AIDS, vol. 21, no. 18, pp. 2561–2564, 2007.
Case Reports in Medicine 7
Available via license: CC BY 4.0
Content may be subject to copyright.
