Persistent gene lymphadenopathy has been well described in patients wi
th seropositivity to the human immunodeficiency virus (HIV). Moreover,
isolated enlargement of the parotid gland and parotid lymphadenopathy
have been noted much more frequently over the past few years. Histolo
gically, these lesions demonstrate follicular hyperplasia, cystic dila
tation of the ducts fined by pseudo-stratified squamous epithelium, an
d lymphocytic infiltrates. They are generally considered to be benign
lymphoepithelial lesions of the parotid or hyperplastic periparotid ly
mph nodes. The relationship of this entity to the AIDS-related complex
(ARC) and the subsequent development of AIDS is not clear. Over the p
ast 7 years, we have seen 50 patients with parotid enlargement in whom
the diagnosis of benign lymphoepithelial lesion was made. Fine-needle
aspiration was performed in 32 patients. Although not conclusively di
agnostic, needle aspirates ruled out primary salivary glandular pathol
ogy. Most patients gave a history of intravenous drug abuse. HIV tests
have been performed on a routine basis only in the last 2 years, and
these were positive in the majority of the patients. Thirty-five patie
nts underwent surgical excision. In the initial 20 patients, we routin
ely performed parotid exploration, identification of the facial nerve,
and superficial parotidectomy. In the last 15 patients, we changed ou
r surgical approach to parotid exploration and excision of the mass in
the tail of the parotid. The exposure of the posterior belly of the d
igastric muscle, with identification and removal of the deep jugular n
ode, has become routine. In each case, we found an enlarged lymph node
in the deep jugular region, which was not clinically palpable preoper
atively. The rate of surgical complications was minimal, and, after re
section of the mass, patients improved symptomatically. If the patient
shows obvious signs of AIDS, a nonsurgical approach with repeated asp
irations should be considered, and treatment with zidovudine offered.