considered as a very low CD4 count.This is in
accordance with data provided in figure 2, where
OHL is correlated with CD4 T cell counts <200/μL.
According to WHO clinical staging of
HIV/AIDS for Adults and Adolescents, patient with
OHL is classified as HIV stage 3, (WHO, 2007)
but
CDC stated that when the number of CD4 cells falls
below 200 cells/mm, the patient is considered as
AIDS. (Greenspan et al., 1984). Diagnosis of AIDS
can also be established when one or more
opportunistic infection occured, regardless of the
CD4 count.
Therefore the patient was diagnosed
with OHL and AIDS.
In order to diagnosed patient with EBV infection,
further examination to obtain EBV in the lesion
needed. This can be done by performing
histopathology, exfoliative cytology, in situ
hybridization (ISH), or PCR examination. The most
common histopathological features of OHL include
hyperparakeratosis, epithelial hyperplasia, koilocyte-
like cells within the prickle cell layer and minimal or
complete absence of inflammatory cells in the
lamina propria. A band-like layer of cells with clear
cytoplasm (ground glass appearance) with basophilic
nuclear inclusions, ballooning of cytoplasm and
intracellular edema can also be seen in the upper
spinous layer (Davis et al., 2017).
In our patient, the result of cytopathology
examination does not specific for OHL. A study
revealed that only 50% of HIV patients with clinical
OHL had nuclear change (Reginald et al., 2017).
Suggestive clinical findings, the typical involvement
of lateral borders, the lack of response to
ketoconazole treatment and the patient’s HIV status
is sufficient to make the diagnosis.
The differential diagnosis of OHL include oral
candidiasis, lichen planus, tobacco-associated
leukoplakia, frictional keratosis, human papilloma
virus–induced oral intraepithelial neoplasia, and oral
squamous cell carcinoma (Radwan Ozcko &
Mendak, 2011). In most instances, OHL can be
diagnosed clinically and does not require a
confirmatory biopsy (Triantos et al., 1997).
OHL is a disease of minimal morbidity that does
not always require intervention. Therapy is indicated
when symptoms become troubling or when it is
associated with HIV infection. Treatments for OHL
when required consist of varying options. Usually
the institution of highly active antiretroviral therapy
(HAART) will reduced viral load and increased CD4
count which help decreasing prevalence of OHL
significantly. Other therapeutic options including
systemic antiviral agents such as acyclovir and
valacyclovir, topical podophyllin, topical retinoids,
cryotherapy and surgical excision (Triantos et al.,
1997; Uihlein et al., 2011).
In our case, the patient was administered
acyclovir 800 mg oral 5 times daily, which is
corresponding with guidelines in the literature, for 2
weeks.After the 1
st
week, the lesion on the lateral
borders had subsided, the therapy was then
continued for another week to make sure the lesion
has totally disappeared. The institution of HAART
could also prevent the recurrence of OHL in this
patient.
4 CONCLUSION
Oral hairy leukoplakia is a predictor and prognostic
factor of HIV infection. It cannot be occured in
immunocompetent patient so immunocompromised
condition which can be caused by HIV must be ruled
out before considering other immunocompromised
etiologies. Oral manifestations are the earliest and
most important indicators of HIV infection. OHL is
often misdiagnosed and thus proper treatment is
delayed.
In early diagnosis of OHL, health care provider
must be cautious for and perform further
examination to establish the diagnosis of HIV
infection. Institution of HAART on HIV-related
OHL patient significantly decline the prevalence of
OHL. Other treatments such as systemic antiviral
accelerate the resolution process. The ability to
recognize early OHL manifestation in patient with
HIV is key to providing optimal and appropriate
care, administer early medical intervention and thus
prolonging patient’s life and improve their quality of
life.
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