World Journal of AIDS, 2011, 1, 63-69
doi:10.4236/wja.2011.13010 Published Online September 2011 (http://www.SciRP.org/journal/wja)
63
Kaposi Sarcoma in HIV Positive Nigerian
Children: A Case Series
Regina Oladokun1*, Bamidele Kolude2, Gabriel Ogun3, Biobele Brown1, Kikelomo Osinusi1
1Department of Paediatrics, University of Ibadan and University College Hospital Ibadan, Ibadan, Nigeria; 2Department of Oral Pa-
thology, University of Ibadan and University College Hospital Ibadan, Ibadan, Nigeria; 3Department of Pathology, University of
Ibadan and University College Hospital Ibadan, Ibadan, Nigeria.
Received June 23rd, 2011; revised July 11th, 2011; accepted July 20th, 2011.
ABSTRACT
Background: HIV associated KS is relatively rare in children and has been reported to be higher in East Africa com-
pared to other regions. Literature on cases of histologically proven Kaposi sarcoma in children with HIV infection in
West Africa is scanty. Case presentation: This communication presen ts three cases of KS seen among children in a pae-
diatric HIV unit. The first case was an eleven year old HIV positive boy who had oral candidiasis that resolved with
treatment and subsequently developed a painless, erythematous swelling at the middle of the dorsum of the tongue with
central loss of papillae. He also had multiple discoid hyperpigmented flat lesions on the legs and soles of the feet. In
addition to switching to second line antiretroviral therapy, he had chemotherapy. The lesions regressed. The second
case was a double orph an who had KS involvement of the right eye , nasal cavity and lymph nodes. The tumour rapidly
progressed and the child died before ART and chemotherapy could be commenced. The last case was a five year old
girl with mild KS of the skin but also had other manifestations of severe HIV disease which she succumbed to. Inci-
sional biopsies of the lesions revealed an invasive epithelial lined vascular tumour destroying the upper layers of
skeletal fibres within the conn ective tissue stroma in keeping with KS. Human Herpes Virus type 8 (HHV8) screen was
also positive for all the cases. Conclusion: A high index of suspicion must be entertained and biopsy of suspicious
muco-cutaneous lesions is necessary to exclude a diagnosis of KS which is an indicator of severity and progression of HIV.
Keywords: Kaposi Sarcoma, HIV Infection, Children, West Africa
1. Introduction
Though Kaposi Sarcoma (KS) is relatively infrequent
among children compared to adults, in some parts of re-
source poor continents such as East Africa and Latin
America, frequent lesions of KS have been documented
among children and had been attributed to endemic
presence of Human Herpes Virus type 8 (HHV8) [1,2].
HIV-associated Kaposi Sarcoma (HIV-KS) is the most
common neoplasm observed in HIV-seropositive sub-
jects [3] and it has been reported in different age groups
of children worldwide presenting predominantly as mu-
cocutaneous disease. The earliest documentation of
childhood KS included a 6 day old neonate and a six
month old infant both born to mothers with HIV/AIDS
[4].
Although cutaneous lesions are the most common
manifestations of KS [5], in 22% of subjects with HIV
KS, the lesion is first seen in the mouth and in 71% of
the subjects with HIV KS the oral cavity will b e affected.
The most common intra oral site is the palate followed
by the lips and the tongue [6]. Among children with
HIV/AIDS in the developing world, the prevalence of
oral lesions vary from country to country, but it is widely
accepted that oral candidiasis is the most common lesion
in children. By contrast, neoplastic lesions that involve
the oral cavity including Kaposi sarcoma are relatively
rare [7,8].
What is known about the aetiology of KS has evolved.
Viruses may play an important role in its aetiopatho-
genesis. The most convincing evidence for viral aetiol-
ogy was proposed following the discovery of DNA se-
quences of HHV8 in KS lesions of virtually all AIDS
patients [9]. HHV8 DNA is seen in higher concentration
in oral fluids than other bodily secretions in subjects with
HIV-KS and this may partly explain the high prevalence
of HIV-KS in the mouth. In a retrospective study [10], it

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series 64
was observed that death rate in subjects with oral HIV-
KS was higher than in subjects with exclusive cutaneous
manifestations [11]. Genetic predisposition was proposed
by Friedman Kien et al. [12] as an aetiological factor
which could be as a result of increased incidence of his-
tocompatibility marker HLA-DR5 in 62% of classic KS
while Windle-Taylor and Shah [13] suggested an envi-
ronmental aetiology due to specific geographic distribu-
tion of the disease. Though HIV is not a direct aetiologi-
cal agent, it provides the environment for opportunistic
factors. Furthermore, other factors including HIV trans-
activating (tat) gene and cytokines such as Oncostatin M
and scatter factor, along with some states of immune-
system compromise are important contributors to the
development of KS [14].
There had not been any previous documentation of
cases of clinical and histologically proven Kaposi sar-
coma in children with HIV infection in Nigeria, [15,16]
This report was therefore necessary to document and to
alert clinicians to the po ssibility of this diagn osis in HIV
infected children.
2. Case Presentation
2.1. Case 1
This 11 year old HIV positive boy who had been on
antiretroviral therapy (ART) for four months was admit-
ted into a paediatric ward of the University College Hos-
pital, Ibadan, Nigeria in June 2008. He was referred on
the suspicion of HIV infection to the Hospital five and a
half months earlier. The HIV rapid test was reactive and
was confirmed by Western blot. HIV infection was also
confirmed in his mother. He had presented with angular
cheilitis and difficulty with eating, facial swelling, per-
sistent cough, bilateral leg swelling, recurrent fever and
generalised non-pruritic hyperpigmented skin lesions.
On examinat i on, he was wa ste d wi th hi s we igh t at 6 8 %
of the median for age. His tongue showed a cream col-
oured plaque at the lateral aspect with erythematous
margin that extended to the oropharynx. He was dysp-
noeic and had lung crepitations. The chest radiograph
showed homogenous opacities on the right mid zone but
the Mantoux test and sputum microscopy for Acid Fast
Bacilli were negative. At this stage, the haematocrit was
22%; CD4 count 14 cells/µl and CD4% 2.2. An abdomi-
nal ultrasound revealed normal sized kidneys with in-
creased echogenicity and coarse echo texture without
intrinsic masses.
Urinalysis showed a specific gravity of 1.012 and pro-
tein (2+), liver function tests revealed hypoproteinaemia
and hypoalbuminaemia but the enzymes were within
normal limits. He was diagnosed then with the World
Health Organization (WHO) Clinical stage 4 HIV disease
with right lobar pneumonia, oropharyngeal candidiasis
(pseudomembranous type) and possible HIV Nephropa-
thy. He commenced first line anti-retroviral therapy (zi-
dovudine, lamivudine & nevirapine) alongside antibiotics
(cefuroxime and gentamycin) and antifungal agents (flu-
conazole). At the end of two weeks, the oropharyngeal
lesion and lung crepitations had resolved and he was
discharged and continued management on outpatient
basis.
Two months later he presented with anorexia, recur-
rent vomiting and difficulty with walking. On examina-
tion, he was pale and had recent appearance of darkish
brown to black multiple maculo-papular pigmented le-
sions on the trunk, lower extremities and a so litary nodu-
lar lesion on the plantar surface of the right foot (Figure
1(a)). There was also an intra-oral, erythematous swell-
ing located centrally on the dorsum of the tongue meas-
uring 3 × 2 cm (Figure 1(b)). The patient admitted that
swelling on the tongue was first noticed two weeks ear-
lier and had increased gradually in size without associ-
ated pain. In view of the anatomical location, central loss
of papillae and associated history of oropharyngeal can-
didiasis, an initial clinical impression of median rhom-
boid glossitis was entertained. This lesion however did
not respond to antifungal therapy. An excisional biopsy
of the tongue lesion was carried out. Special stain with
Gomori’s methenamine silver failed to demonstrate fun-
gal hyphae. Haematoxylin and eosin stained histologic
sections of both the tongue and skin lesions revealed a
cellular neoplasm composed of spindle cells with slit-like
spaces containing red blood cells (Figure 2(a)). There
was deep skeletal muscle invasion by tumour cells, with
chronic inflammation in the upper corium which was in
keeping with KS (Figures 2(b) and 2(c)).
Additionally, the leg swelling had persisted and the
serum creatinine became elevated. A renal biopsy was
carried out and histology revealed moderate cystic dila-
tion with mild degeneration of both proximal and distal
tubules and focal segmental glomerulosclerosis. Based
on these features the diagnosis of HIV associated neph-
ropathy was reinforced. CD4 count and CD4% at this
point was 29 and 4.9% respectively while the haema-
tocrit was 28%.
The tumour cells showed strong granular nuclei stain-
ing in keeping with KS HHV-8 (Figure 2(d)). He was
readmitted and switched to second line antiretroviral
therapy (Lamivudine, Didanosine, Lopinavir/ritonavir).
He was monitored for toxicity and subsequently chemo-
therapy was added to the treatment as stipulated in the
National guideline for treatment of HIV associated KS
[17] The chemotherapy regimen consisted of two
weekly courses of Adriamycin for 6 cycles. Two months
after the commencement of chemotherapy, the tongue

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series65
ab
c
d
e
Figure 1. Case 1. (a) Initial nodular lesion on the plantar
surface of the right foot; (b) Initial multiple coalescent
nodular haemorrhagic tongue lesions; (c) Plantar lesion 2
months after commencing chemotherapy; (d) KS lesion on
sole of right foot, post chemotherapy; (e) KS lesion on the
tongue post treatment.
Figure 2. Histology and KS HHV-8 staining of tumour cells.
(a) Haematoxylin and eosin section (× 200) show supe rficial
dermal vascular and spindle cell proliferation; (b) Promi-
nent staining of the vascular endothelia lining with CD 31
and involvement of the superficial dermis (× 200); (c) CD 34
positive endothelial vascular channel of a dermal KS rami-
fying around a sweat gland—block arrow (× 200); (d) KS
HHV-8 staining of the tumour cells with strong granular
nuclei staining (× 400).
lesion had regressed completely (Figure 1(c)) and the
plantar lesion had also flattened (Figure 1(d)) and was
no longer tender. At the time of this report, nearly three
years after, the tongue and skin lesions had not recurred
(Figures 1(d) and 1(e)) and the serum electrolyte, urea
and creatinine are normal. He is regular on second line
antiretroviral therapy and has since achieved complete
viral suppression (<200 copies/ml) with the latest CD4+
count of 760 cells/µl.
2.2. Case 2
This was a 9 year old boy that presented in February,
2009 at the same health facility with cough of 3 months
duration, neck and scalp swellings and protrusion from
the right eye of 2 months duration. His parents had died
of wasting disease within the previous 6 months before
his presentation. The causes of death were not confirmed
before demise. The patient had two siblings; the youngest
had died in infancy while the immediate younger sibling
was alive. Both surviving children were living with their
maternal grandmother.
The swellings over the scalp and neck progressively
increased in size. The growth on the right eye was
painless with associated watery eye discharge and grad-
ual loss of vision.
At presentation, he was wasted, small for age and had
extensive scaly lesions on the scalp. He was mildly pale,
afebrile, anicteric, had generalized lymphadenopathy and
no peripheral oedema. He had a fungating nodular mass
protruding from the right eye and other nodular sw ellings
on the right temporal region (Figures 3(a)-(c)) and lower
limbs. His weight was 17 kg (58.6% of expected) and his
height was 111 cm being 84.7 per cent of the median for
his age indicative of stunting.
Significant findings on physical examinations included
noisy breathing, intercostal recessions with a respiratory
rate of 36 breaths per minute, reduced air entry on the
left lower lung zone, bronchial breath sounds on the right
upper and mid lung zones. There was hepatomegaly of 4
cm below the right costal margin.
The chest radiograph showed collapse of the right up-
per lobe with compensatory emphysema of the right
middle and lower lobes and the left lung. Mantoux test
and sputum microscopy for Acid Fast Bacilli were nega-
tive. His haematocrit was 19% and serum electrolytes,
urea and creatinine were within normal limits. Rapid
HIV test was reactive and was confirmed by Western
Blot. His CD4 count was 72 cells/ul (0.2%) and viral
load was 168,041 copies/ml. He tested positive to Hepa-
titis C antibody and negative t o Hepatitis B surface antigen.
He was diagnosed to have WHO clinical stage 4 HIV
Infection with possible disseminated Tuberculosis (pul-
monary, abdominal, lymph node), Kaposi Sarcoma and

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series 66
ab
a
c
Figure 3. CASE 2. (a) Nodular anterior and posterior cer-
vical neck swellings; (b) Exopthalmos of the right eye; (c)
Corneal tumour and nodular swelling on the right temporal
region.
tinea capitis. He received antibiotics for suspected pyo-
genic pneumonia, ketoconazole, Cotrimoxazole for treat-
ment of Pneumocystis pneumonia and anti tuberculosis
therapy. ART was commenced two weeks later. However,
his clinical status continu ed to d eteriorate with worsening
respiratory distress and nodular lesions extending to the
left eye, left nostril, palate and the upper limbs that bled
to touch. Histology of the lymph node and skin nodule
were in keeping with KS and the HHV8 screen was also
positive.
While he was being worked up for chemotherapy; he
developed copious serosanguinious discharges from the
nostrils and petechiae haemorrhages on the skin. He went
into cardiopulmonary arrest for which resuscitative ef-
forts were unsuccessful.
2.3. Case 3
This was a five year old girl who presented to the UCH,
Ibadan in September 2010 with a 3 month’s history of
recurrent fever, cough, weight loss and diarrhoea. Her
weight was 11 Kg (60% of expected) and the height was
105 cm (50th percentile). The mid upper arm circum-
ference was 11.2 cm. She was chronically ill with florid
oral thrush, angular stomatitis, generalized lymphade-
nopathy, crepitations in the lungs and hepatomegaly.
HIV infection was confirmed by Western Blot. Her
mother and younger sibling were also confirmed to have
HIV infection. Her CD4 coun t was 4 cells/µl (1.4%). She
was transfused with packed red cells on account of a
haematocrit of 11%. She also had severe hypokalaemia
(1.9 mmol/l) which was corrected and symptomatic hy-
pocalcaemia that manifested as carpopedal spasm that
resolved with calcium therapy. Haemoglobin genotype
could not be ascertained as she had received blood trans-
fusion shortly b efore her presentation to UCH. An initial
chest radiograph was normal, mantoux test was negative,
and gastric washings for AFB was also negative. ART
was commenced two weeks later using a combination of
Zidovudine, Lamivudine and Efavirenz. She also re-
ceived nutritional rehabilitation with ready to use foods.
As a result of her continued poor clinical status and fail-
ure to improve on antibiotics, a repeat chest radiograph
later showed bilateral opacities on account of which she
was treated with antituberculosis therapy consisting of
Rifampicin, Isoniazid, Pyrazinamide and Ethambutol.
Four weeks into admission, two hyperpigmented no-
dular non-tender lesions measuring 1.5 cm in the widest
diameter were observed over the left temporal region of
the face which was histologically confirmed as Kaposi
sarcoma (Figure 4). The KS HHV8 screen was also
positive. She had minimal improvement in her general
condition initially but later deteriorated with develop-
ment of jaundice and an episode of generalized tonic-
clonic seizure. The cerebrospinal fluid analysis was not
suggestive of meningitis or meningoencephalitis. On
account of suspected drug toxicity the antituberculosis
and antiretroviral drugs were discontinued. However she
died shortly after while further investigations into this
were on going.
3. Discussion
These cases of histological proven Kaposi sarcoma in
these children with confirmed HIV infection in this re-
port illustrate that KS occurs in children not only in East
Africa [6] and Southern America [4], but in other parts of
Africa including Nigeria. In a study of AIDS associated
KS in Nigeria over a 10 year period, it was reported that
there was no case of childhood involvement among the
patients [18]. This was thought to be from misdiagnosis
as KS may be confused with lesions including congenital
haemangioma, dysplastic naevi and dermatofibromas.
Routine tissue biopsy of suspicious lesions in children
would increase the detection of KS among HIV positive
children with skin lesions. The three cases in this report
had KS involvement of the skin. However, KS may also
affect the less obvious organs in the body and also affect

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series67
Figure 4. CASE 3. Hyper pigmented nodular lesions on the
right temporal, maxillary and mandibular regions indicated
with black arrows.
multiple sites. Multiple sites of KS were seen in almost
45% of the children with HIV and AIDS with the skin
being the most common site, occurring either alone or in
combination with other sites. The skin was involved in
over 57% of the children in the series reported from
South Africa [19]. In addition, as a result of the high
burden of tuberculosis and other opportunistic infections,
KS of the lungs may be misdiagnosed [20]. The issue is
further complicated by the fact the chest radiograph
findings may be unspecific as it could mimic a myriad of
other infectious and non infectious diseases. Radio-
graphic findings of pulmonary Kaposi’s sarcoma have
been described in HIV positive children. The typical
features were reported to include hilar lymphadenopathy,
diffuse bilateral peri-hilar and lower zone infiltration, air
space and reticular opacification, and effusions [21]. The
second case in our report may well have had pulmonary
involvement of KS. This could not be confirmed as a
post mortem could not be carried out.
The children in this report were all older than 5 years
of age and the mode of transmission of HIV was pre-
sumably vertical as they had no other obvious risk factors
for HIV infection. Though the onset of HIV symptoms
was delayed, the progression of the disease was rapid.
Other reports of KS in the paed iatric age grou p were also
in older children who had had long standing disease [22].
Children known to have had prior blood transfusions
probably resulting in HIV infection had also been re-
ported to have KS and did not have features that might
distinguish them from those who acquired HIV from
their mothers [2]. It is to be noted also that our patients
had severe immunosuppression with very low CD4+
counts. In a larger retrospective paediatric study, a simi-
lar observation was made where all 61 but two cases had
a severely compromised immunity [19].
Candidiasis is the most frequent oral feature of HIV/
AIDS in children and some authors have separated cases
presenting with angular cheilitis or pseudomembranous
features from other variants [22,23]. The first case pre-
sented had pseudomembranous type in the oropharynx
which respo nded to fluconazole an antifungal agent. Due
to the previous episod e of oropharyngeal candidiasis and
the anatomical location of the tongue lesion, an initial
impression of median rhomboid glossitis was entertain ed
but special stain with Gomori’s methenamine silver
failed to demonstrate fungal hyphae. Other differential
diagnoses of depapillated midline nodular tongue swell-
ings include lingual thyroid, gumma of tertiary syphilis,
granuloma of tuberculosis and granular cell tumour. All
the above were excluded with the outcome of the tissue
biopsy of the tongue that had been described earlier. The
histological features coupled with the skin lesions that
became more obvious led to diagnosis of Kaposi’s sar-
coma.
Although neoplasms are rare oral manifestations of
children infected with HIV/AIDS [24], the tendency to
develop oral KS and oral hairy leukoplakia has been
known to increase with age due to longer exposure to
HHV-8 and EBV [25]. The three children in the study
had evidence of HHV-8 co-infection. The pathomecha-
nism of development of KS following HSV infection is
uncertain but it is postulated that HHV8 encodes several
genes that have capacity to stimulate angiogenesis by
inducing angiogenic phenotype transformation of HHV-8
infected cells or by production of inflammatory cytokines,
chemokines and growth factors that can activate and
promote angiogenesis [5]. In a study of KS in childhood
in Uganda, immune dysfunction and local inflammation
were implicated as predisposing factors since prodromal
symptoms of HIV infection were present in the majority
and 39% of patients had an infection in a site later in-
volved with KS [2].
Patients with KS need to be diagnosed and treated with
ART promptly in order to reduce mortality as survival
correlates significantly with the antiretroviral treatment
[19]. A challenge in the management of these patients
would be monitoring for toxicities that could result from
drug interactions from the combination of antiretroviral
therapy, anti tuberculosis regimen, chemotherapy, anti-
fungals and other drugs that may be requir ed. A twofo ld
risk of developing opportunistic infections had been re-
ported in HIV infected patients with Non-Hodgkin’s
lymphoma who had been treated with systemic chemo-
therapy [26]. The risk for opportunistic infections in
HIV-infected patients with KS is also increased while

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series 68
receiving chemotherapy [27]. In many studies which
were mainly in adults, Kaposi’s sarcoma Immune Re-
constitution Inflammatory Syndrome (IRIS) had also
been reported [28,29].
4. Conclusions
KS occurs in children with HIV infection in Nigeria,
Western Africa though it appears to be uncommon when
compared with the occurrence in some other African
sub-regions. With the increased availability of antiretro-
viral therapy, which is associated with better survival,
there should be a high index of suspicion for KS in HIV
infected children with suggestive signs as its presence is
an indication of severity and progression of the disease.
Biopsy of such lesions in muco-cutaneous and other ac-
cessible sites is necessary to exclude a diagnosis of KS.
Early diagnosis for prompt institution of therapy is nec-
essary to improve the chances of survival.
REFERENCES
[1] K. Ranganathan and R. Hemalatha, “Oral Lesions in HIV
Infections in Developing Countries: An overview,” Ad-
vances in Dental Research, Vol. 19, No. 1, 2006, pp. 63-
68. doi:10.1177/154407370601900113
[2] J. L. Ziegler and E. Katongole-Mbidde, “Kaposi’s Sar-
coma in Childhood: An Analysis of 100 Cases from
Uganda and Relationship to HIV Infection,” International
Journal of Cancer, Vol. 65, No. 2, 1996, pp. 200-203.
doi:10.1002/(SICI)1097-0215(19960117)65:2<200::AID-
IJC12>3.0.CO;2-H
[3] L. Feller and J. Lemmer, “HIV-Associated Kaposi’s Sar-
coma: Pathogenic Mechanisms,” Oral Surgery Oral Me-
dicine Oral Pathology Oral Radiology and Endodontics,
Vol. 104, No. 4, 2007, pp. 521-529.
doi:10.1016/j.tripleo.2006.08.015
[4] K. P. Manji, H. Amir and I. Z. Maduhu, “Aggressive
Kaposi’s Sarcoma in a 6-Month-Old African Infant: Case
Report and Review of the Literature,” Tropical Medicine
& International Health, Vol. 5, No 2, 2000, pp. 85-87.
doi:10.1046/j.1365-3156.2000.00523.x
[5] A. K. Agarwal, G. Zamzachin, Y.Mohen, M. Y. Singh
and N. Singh, “AIDS Related Kaposi’s Sarcoma—Like
Lesion,” Indian Journal of Dermatology, Vol. 62, No. 2,
1996, pp. 129-131.
[6] J. B. Epstein, R. J. Cabey and M. Glick, “Oral Malignan-
cies in HIV Disease: Changes in Disease Presentation,
Increasing Understanding of Molecular Pathogenesis and
Current Management,” Oral Surgery Oral Medicine Oral
Pathology Oral Radiology, and Endodontics, Vol. 100,
No. 5, 2005, pp. 571-578.
doi:10.1016/j.tripleo.2005.01.015
[7] P. Khongkunthlan, M. Grote, W. Isaratanan, S. Plyawo-
rawong and P. A. Reichart, “Oral Manifestations in 45
HIV-Positive Children from Northern Thailand,” Journal
of Oral Pathology & Medicine, Vol. 30, No. 9, 2001, pp.
549-552. doi:10.1034/j.1600-0714.2001.300907.x
[8] I. D. Miziara, B. C. Araújo Filho and R. Weber, “Oral
Lesions in Brazilian HIV-Infected Children Undergoing
HAART,” International Journal of Pediatric Otorhi-
nolaryngology, Vol. 70, No. 6, 2006, pp. 1089-1096.
doi:10.1016/j.ijporl.2005.11.010
[9] I. Lager, M. Altini, H. Coleman and H. Ali, “Oral Ka-
posi’s Sarcoma: A Clinicopathologic Study from South
Africa,” Oral Surgery Oral Medicine Oral Pathology
Oral Radiology, and Endodontics, Vol. 96, No. 6, 2003,
pp. 701-710. doi:10.1016/S1079-2104(03)00370-6
[10] M. M. Taylor, B. B. Chohan, L. Lavreys, W. Hassan, M.
L. Huang, L. Corey, R. Ashley Morrow, B. A. Richardson,
K. Mandaliya, J. Ndinya -Achola, J. Bwayo and J. Kreiss,
“Shedding of Human Herpes Virus 8 in Oral and Genital
Secretions from HIV-1 Seropositive and Seronegative
Kenyan Women,” Journal of Infectious Diseases, Vol.
190, No. 3, 2004, pp. 484-488. doi:10.1086/421466
[11] B. Rohrmus, E. M. Thoma-Greber, M. Rocken and J. R.
Bogner, “Outlook in Oral and Cutaneous Kaposi’s Sar-
coma,” Lancet, Vol. 356, No. 9248, 2000, p. 2160.
doi:10.1016/S0140-6736(00)03503-0
[12] A. E. Friedman-Kien, L. J. Laubenstein, P. Rubinstein, E.
Buimovici-Klein, M. Marmor, R. Stahl, I. Spigland, K. S.
Kim and S. Zolla-Pazner, “Disseminated Kaposi’s Sar-
coma in Homosexual Men,” Annals of internal medicine,
Vol. 96, No. 6, 1982, pp. 693-700.
[13] P. C. Windle-Taylor and N. Shah, “Oropharyngeal Ka-
posi’s Sarcoma: Report of Two Cases and Review of the
Literature,” Journal of Laryngology and Otology, Vol. 97,
No. 11, 1993, pp. 1065-1071.
[14] C. Oji and F. Chukwuneke, “Clinical Evaluation of Ka-
posi Sarcoma in HIV/AIDS Patients with Orofacial Le-
sions in Enugu, Nigeria,” Journal of Oral Maxillofacial
Surgery, Vol. 66, No. 7, 2008, pp. 1362-1365.
doi:10.1016/j.joms.2007.08.049
[15] M. I. Adurogbangba, G. A. Aderinokun, G. N. Odaibo, O.
D. Olaleye and T. O. Lawoyin, “Oro-Facial Lesions and
CD4 Counts Associated with HIV/AIDS in an Adult
Population in Oyo State, Nigeria,” Oral Diseases, Vol. 10,
No. 6, 2004, pp. 319-326.
doi:10.1111/j.1601-0825.2004.01036.x
[16] G. A. Agbelusi and A. A. Wright, “Oral Lesions as Indi-
cators of HIV Infection among Routine Dental Patients in
Lagos, Nigeria,” Oral Diseases, Vol. 11, No. 8, 2005, pp.
370-373.
[17] Federal Ministry of Health of Nigeria, “National Guide-
lines on Cancer Chemotherapy,” Federal Ministry of
Health of Nigeria, 2008.
[18] N. Mbah, I. H. Abdulkareem and A. Panti, “AIDS-Asso-
ciated Kaposi’s Sarcoma in Sokoto, Nigeria,” Nigerian
Journal of Clinical Practice, Vol. 11, No. 3, 2008, pp.
181-184.
[19] D. C. Stefan, D. K. Stones, L. Wainwright and R. Newton,
“Kaposi Sarcoma in South African Children,” Pediatric
Blood Cancer, Vol. 56, No. 3, 2011, pp. 392-396.
doi:10.1002/pbc.22903

Kaposi Sarcoma in HIV Positive Nigerian Children: A Case Series 69
[20] A. Mosam, J. Aboobaker and F. Shaik, “Kaposi’s Sar-
coma in Sub-Saharan Africa: A Current Perspective,” Cur-
rent Opinion in Infectious Diseases, Vol. 23, 2010, pp.
119-123.
[21] S. Theron, S. Andronikou, R. George, J. du Plessis, P.
Goussard, M. Hayes, A. Mapukata and R. Gie, “Non-In-
fective Pulmonary Disease in HIV-Positive Children,”
Pediatric Radiology, Vol. 39, No. 6, 2009, pp. 555-564.
doi:10.1007/s00247-009-1156-2
[22] C. Okunseri, V. Badner, A. Wiznia and M. Rosemberg,
“Prevalence of Oral lesions and Percent CD41+ T-Lym-
Phocytes in HIV Infected Children on Antiretroviral
Therapy,” AIDS Patient Care and STDS, Vol. 17, No. 1,
2003, pp. 5-11. doi:10.1089/108729103321042863
[23] A. Chan, A. Milnes, S. M. King and S. Read, “The Rela-
tionship of Oral Manifestations to Parameters of Immune
Function and CDC Stage in Children Born to HIV Posi-
tive Women,” In: Pediatric AIDS and HIV Infection: Fe-
tus to Adolescent, Williams & Wilkins, Baltimore, 1994,
pp. 101-107.
[24] B. Ensoli, R. Gendelman, P. Markham, V. Fiorelli, S.
Colombini, M. Raffeld, A. Cafero, H. K. Chang, J. N.
Brady and R. C. Gallo, “Synergy between Basic Fibro-
blast Growth Factor and HIV-1 Tat Protein in Induction
of Kaposi’s Sarcoma,” Nature, Vol. 371, 1994, pp. 674-
680. doi:10.1038/371674a0
[25] M. W. Kline, “Oral Manifestations of Pediatric Human
Immunodeficiency Virus Infection: A Review of the Lit-
erature,” Pediatrics, Vol. 97, No. 3, 1996, pp. 380-388.
[26] J. A. Sparano, X. Hu, P. H. Wiernik, C. Sarta, D. M.
Reddy, L. Hanau and D. H. Henry, “Opportunistic Infec-
tion and Immunologic Function in Patients with Human
Immunodeficiency Virus- Associated Non-Hodgkin’s Ly m-
phoma Treated with Chemotherapy,” Journal of the Na-
tional Cancer Institute, Vol. 89, No. 4, 1997, pp. 301-307.
doi:10.1093/jnci/89.4.301
[27] A. Plettenberg, U. van Dyk, A. Stoehr, H. Albrecht, H. J.
Stellbrink, J. Berger and W. Meigel, “Increased Risk for
Opportunistic Infections during Chemotherapy in HIV-In-
fected Patients with Kaposi’s Sarcoma,” Dermatology,
Vol. 194, No. 3, 1997, pp. 234-237.
doi:10.1159/000246109
[28] D. M. Murdoch, W. D. Venter, C. Feldman and A. Van
Rie, “Incidence and Risk Factors for the Immune Recon-
stitution Inflammatory Syndrome in HIV Patients in
South Africa: A Prospective Study,” AIDS, Vol. 22, No. 5,
2008, pp. 601-610. doi:10.1097/QAD.0b013e3282f4a607
[29] E. Letang, J. Almeida, E. Ayala, I. E. White, C. Carrilho,
R. Bastos, T. Nhampossa, C. Menéndez, T. B. Campbell,
P. L. Alonso and D. Naniche, “Predictors of Immune Re-
constitution Inflammatory Syndrome-Associated with
Kaposi Sarcoma in Mozambique: A Prospective Study,”
Journal of Acquired Immune Deficiency Syndrome, Vol.
53, No. 5, 2010, pp. 589-597.